Eczema

Dr.APARNA.S. BHMS, Thiruvananthapuram

INTRODUCTION

Dermatology is one of the most important disciplines of medicine, where a disease apprises itself over the skin .The diseases affecting the skin always create mental stress to the patients because of external appearance. So its study, have an important place in the practice of medicine.                                                                        

Eczema is one of the most common skin diseases affecting humanity from time immemorial. Eczema can very well be called the first illness man could have suffered. We find its descriptions even in the most ancient writings. Perhaps the primitive men feared skin diseases more or less the way we do nowadays with regards to Cancer or AIDS.

Eczema or dermatitis is a reaction pattern that presents with variable clinical and histological findings and is the final common expression for a number of disorders including atopic dermatitis, allergic and irritant contact dermatitis, dyshydrotic eczema, nummular eczema etc. Primary lesions may include papules, erythematous macules and vesicles which can coalesce to form patches and plaques. In severe eczema, secondary lesions from infection or excoriation, marked by weeping and crusting may predominate. Long standing dermatitis is often dry and is characterized by thickened, scaling skin (lichenification).

According to Homoeopathy, it is the outward reflection of a deranged internal economy. The most significant aspect of eczema or rather “itch”, is its link with the Theory of Chronic Diseases and miasms especially Psora. Dr.Samuel Hahnemann, the Father of Homoeopathy believes that 7/8ths of all the chronic maladies spring from Psora, a constitutional predisposition to  a multitude of illnesses , the origin of which can be traced back to a suppressed itch, perhaps , in the preceding generations.

According to Dr.Hahnemann, “The oldest monuments of history which we possess show the Psora even then in great development. Moses, 3400 years ago pointed out several varieties. In Leviticus, (chap 13&21, verse 20) he speaks of bodily defects, which must not be found in a priest, who is to offer sacrifice, malignant itch is designated by the word Garab, which the Alexandrian translators(in the Septuagint) translated with Psora agria, but the Vulgate with scabies jugis. The Talmudic interpreter, Jonathan, explained it as dry itch spread over the body; while the expression Yalephed, is used by Moses for lichen, tetters, herpes. The commentators in the so-called English Bible-work also agree with this definition, Calmet among others, saying:

“Leprosy is similar to an inveterate itch with violent itching”. The ancients also mention the peculiar, characteristic, voluptuous itching, which attended itch then as now, while after the scratching, a painful burning follows; among others Plato, who calls glykypikron, while Cicero remarks the dulcedo of scabies. At that time and later on among the Israelites, the disease seems to have mostly kept the external parts of the body for its chief seat. This was also true of the malady as it prevailed in uncultivated Greece, later in Arabia, and lastly, in Europe during the Middle Ages.”

The nature of this miasmatic itching eruption always explained essentially the same. It is identical, therefore, with the ancient form of leprosy; with the “St. Antony’s Fire” or malignant erysipelas, which prevailed in Europe for several countries and then reassumed the form of leprosy, which was brought back by returning crusaders in the thirteenth century. After that it spread more than ever. It was gradually modified by greater personal cleanliness, more suitable clothing and general improvement in hygienic conditions, until it was reduced to a “common itch”, which could be and more easily removed from the skin by external treatment. But as Hahnemann points out the state of mankind, was not improved thereby; in many respects it grew far worse.

SKIN: EMBRYOLOGY

The skin is derived from three diverse components:

a)      The epidermis is derived from the surface ectoderm. At first, it is single layered. By proliferation, it gives rise to typical stratified squamous epithelium. Many of the superficial layers are shed off. These get mixed with sebaceous glands’ secretions to form a whitish sticky substance (vernix caseosa) which covers the skin of the newborn infant. It has a protective function.

b)      The melanoblasts or dendritic cells of the epidermis are derived from the neural crest.

c)      The dermis is formed by the condensation & differentiation of mesenchyme underlying the surface ectoderm. This mesenchyme is believed to be derived from the dermatome of the somites.

The line of junction between dermis and epidermis is at first straight. Subsequently, the epidermis shows regularly spaced thickenings that project into the dermis. The portions of the dermis intervening between these projections form the dermal papillae. Later, surface elevations (epidermal ridges) are formed by further thickening of the epidermis in the same situation.

NAIL

They develop from the surface ectoderm, the tip of which thickens to form a primary nail field. Subsequently, this thickening migrates from the tip of the digit onto its dorsal aspect. The cells in the most proximal part of the nail field proliferate to form the root of the nail. Here the cells of the germinal layer multiply to form a thick layer of cells called the germinal matrix. As the cells in this matrix multiply, they are transformed into the nail substance.

HAIR

It is derived from the surface ectoderm. At the site, where a hair follicle is to form, the germinal layer of the epidermis proliferates to form a cylindrical mass that grows down into dermis. The lower end of this down growth becomes expanded and is invaginated by a condensation of mesoderm, which forms the papilla. The hair itself is formed by a proliferation of germinal cells overlying the papilla. As the hair grows to the surface, the cells forming the wall of the down growth surround it and form the epithelial root sheath. An additional sheath is formed by surrounding mesenchymal cells. A typical hair follicle is thus formed.

SEBACEOUS GLANDS

It is formed as a bud arising from the ectodermal cells forming the wall of a hair follicle.

SWEAT GLANDS

It develops as a down growth from the epidermis. The down growth is at first solid, but later canalized. The lower end is coiled and forms the secretory part of the gland.

MAMMARY GLANDS

Developmentally, they are derived from sweat glands and therefore, it lies in the superficial fascia. The epithelial mammary bud appears at the 35^th day of the intrauterine life. By the 37^th day, a series of mammary bud extending on either side of the midline on the ventral surface of the trunk, extending from axilla to the inguinal region develops. These are called mammary ridges or milk line. Most of the line soon disappears. Each mammary gland develops from a part of the line that overlies the pectoral region. From each mammary bud, 16-20 solid outgrowths arise and grow into the surrounding dermis. Then the mammary bud as well as the outgrowth becomes canalized. Terminal parts of the outgrowths proliferate to form the secretory elements of the gland.

The proximal elements of each outgrowth, forms one lactiferous duct. The ducts at first open into a pit, formed by the cavitations of the original epithelial thickening. This pit is called the mammary pit. The growth of the underlying mesoderm progressively pushes the wall of the pit outwards, until it becomes elevated above the surface and forms the nipple.

SKIN: ANATOMY

The skin is the protective covering of the body. With all its specialized derivatives, it makes up the integument, which covers the entire surface of the human body.

The skin is composed of a superficial epithelial layer- the EPIDERMIS and an underlying connective tissue layer, the DERMIS/CORIUM. Beneath the corium, is another connective tissue layer, the HYPODERMIS or subcutaneous layer. The free surface of the epidermis is marked, by a network of linear furrows and ridges.

Structure of epidermis

The epidermis is composed of non vascular stratified epithelium. Its usual thickness is between 0.07 mm&0.12mm.In soles and palms; it may range from 0.8-1.4mm. The epidermis is mainly divided into:

a)      Keratinizing /Malphigian system(keratinocytes) which forms the bulk

b)      Pigmentary system(melanocytes) which produce the pigment

In addition to keratinocytes, melanocytes, Langerhan cell& indeterminate cell in the epidermis, Merkel cell/Haascheiben/touch cells are found at the base of the epidermal rete ridges and they are in contact with nerve fibrils. They are mostly present in palms, soles, nail beds, oral & genital epithelium and act as slow touch receptors.

The main layers of epidermis, seen in microscopically in a section perpendicular to the skin surface are:

1. Stratum germinativum: This is the deepest portion of the epidermis and is composed of columnar cells placed perpendicular to the skin surface. The whole of the epidermis germinates from this stratum, hence the name “stratum germinativum”. Any trauma to this layer would result in scarring, while the layers above heal without scarring. The basal layer is the site for cellular multiplication. More and more cells are formed and pushed off to the superficial layers. Some of the cells contain melanin. Melanoblasts / melanocytes have branching processes ramifying between the other cells. These appear non- pigmented.
2. 2. Stratum malphighii or the prickle cell layer: It is superficial to basal layer and is composed of several layers of polyhedral connected to each other by intracellular bridges. Electron microscopic studies, have revealed, that adjacent epidermal cells have at their point of contact, areas of thickened membranes. These are called desmosomes. Half size desmosomes occur on the undersurface of the basal cells, which plays an important role in anchoring the epidermis to dermis.
3. 3. Stratum granulosum: It is superficial to the stratum malphighii. It is composed of flat, fusiform cells, which are 1-3 layers thick. These contain irregular layers of keratohyalin and lysosomal enzymes and cystine rich proteins. Above the top of the prickle cell layer, near the granular cell layer, lamellar granules/keratinosomes/Odland bodies are found. These Odland bodies take part in the barrier function of the epidermal permeability. Granular contents of the Odland bodies, are discharged, into the intercellular space, below the cornified cell layer and form an effective waterproof barrier.
4. 4. Stratum lucidum: Superficial to the stratum granulosum is the pale, wavy-looking layer known as stratum lucidum. It is formed by many layers of flattened and closely packed cells whose outlines have become quite indistinct and the nuclei have disappeared. This layer contains refractile droplets of eleidin.
5. 5. Stratum corneum: It is the most superficial layer, the outer surface of which is exposed to the atmosphere. It consists of many layers of non nucleated, flattened, cornified cells. Almost all the cellular structure is lost. It is this layer, which becomes thicker with the application of intermittent mechanical pressure. This layer is thickest on the palms of the hands and soles of the feet, but thinnest on lips, glans penis and the eyes. Electron microscopic studies, shows no organelles/nuclei but tonofibrils are seen embedded in a dense structure less matrix. These tonofibrils at the final stage are considered as mature fibrous protein keratin. Epidermal horny layer contains keratohyalin cement and is referred to as soft keratin. Hard keratin is present in nails and hair.
6. 6. Dendritic cells of the epidermis: These are the melanocytes, Langerhan’s cells and indeterminate cells. Melanocytes are normally present in 1:5 to 1:10 to the epidermal basal cells. Langerhan cells play an important part in antigen transport between the surface of the epidermis and regional lymph nodes. Time taken for the basal cells to reach the final maturation stage of horny cells is about 4-5 weeks. It varies from 72 hours-7 days, depending on the stimulus. Time of maturation decreases during stress, inflammation and psoriasis, when mitotic activity is increased.

Basement membrane

It forms the junction between epidermis and dermis. Electron microscopic studies show half  desmosomes which anchor basal cells to basal lamina. Extending from the basal cell membrane is anchoring dermal filaments. Pemphigoid antigen and laminin are located between the basal cell and basal lamina. This area is 35-45mm thick called lamina lucida. The basement membrane is considered as a porous, semi permeable filter which permits exchange of fluid and cells between the epidermis and dermis. It is made up by Type IV collagen. It is a PAS-positive membrane.

Structure of the dermis(cutis vera or corium)

Dermis is profusely supplied with blood vessels. It is divided into papillary and reticular dermis. It contains connective tissue fibres, cells and all dermal appendages. Connective tissue is mainly formed by 3 components – collagen fibres, elastic fibres, and ground substance. The most abundant constituent is collagen. All these are produced by fibroblast. Beneath the basement membrane are distributed many blood vessels forming a capillary network which ends up as a loop into the dermal papillae. These papillae are microscopic finger-like processes projecting into the epidermis which is moulded over and attached to them. These projections are called rete ridges. The connective tissue cells in the dermis are spindle shaped. Thickness of the dermis is 1-3mm.

On microscopic section, in addition to the above structures, hair follicles, sweat & sebaceous glands, plain muscle fibres, Pacinian and Meissner’s corpuscles are seen. Adipose tissues are present mostly in deeper parts. There are a few round cells, an occasional fibrocyte and few pigment-carrying histiocytes called melanophores. There are rich capillary beds in the papillae and around the appendages and in sub-papillary plexus. Deep reticular plexus is less rich. In the deeper layer of dermis, there is arterio-venous anastomosis (Suquet-Hoyer canal) surrounded by sphincter-like group of smooth muscles under autonomic control and ovoid smooth cells known as glomus cells. Glomus cells are under the control of sympathetic nervous system. A small nerve is associated with every glomus and they respond to various pharmacologic agents and cause vasoconstriction.

Skin is richly innervated by myelinated and non-myelinated sensory fibres and via non-myelinated autonomic fibres supplying blood vessels and appendages. Conspicuous nerve supply consists of plexus in the papillae, Meissner’s corpuscle, Pacinian corpuscles, and Merkel’s disc and nerve endings in basal layer of the epidermis.

SEBACEOUS GLANDS

They are scattered all over the integument except palms of the hand, soles and sides of the feet. They occur in association with hair follicles except in eyelids, lip margins, external auditory meatus, nipples, and anus and around external genitalia, as at these sites, they are more superficial. They are numerous and large on scalp, forehead, ears, face, sterna and interscapular regions. In hairy portions, the ducts open into hair follicles otherwise directly on the skin surface. One or more glands maybe attached to one hair follicle. Meibomian glands, mammary glands and smegma glands of penis are modified sebaceous glands. Perspiration and hot climate stimulates sebum production. They are more active at and after puberty, during menstruation and pregnancy.

SWEAT GLANDS

They are of two types:

1. Eccrine glands: They are ordinary, small-sized sweat glands which are distributed all over the skin except on the bed of nails, lip margins and glans penis. Over 3 million sweat units are present at birth.
2. Apocrine glands: They occur in axillae, areola and nipples of breasts, umbilicus, around the anus and genitalia. Their glandular portion is very large, 3-5mm in diameter. The myoepithelial cells are highly developed and more abundant in these glands. They are specialized sweat glands and their secretion is odoriferous with a secondary sexual significance (pheromone).

HAIR

It is found in every body part except palms, soles, dorsal surface of terminal phalanges, inner surface of labia, prepuce and glans penis. There are 3 types of hair:

a)       Long, medullated, pigmented hair seen on scalp

b)       Short ,fine, non medullated and non pigmented “lanugo” hair seen in women, children, face and trunk of adults(vellus hair)

c)       Thick bristles seen in the nose and ear.

Hair grows about 1-2 cm per month. Hair follicle and its hair can be anatomically, divided into 3 segments: – infundibulum, isthmus and inferior. The lower part of the hair is the site of growth. Hair growth is cyclical consisting of 3 phases- growing (anagen), involutionary (catagen) and resting (telogen).

NAILS

These are semi-transparent, plate-like horny structures, covering the dorsal surfaces of the distal phalanges of the fingers and toes. The proximal edge of the nail is known as the root nail. The visible portion of the nail is the nail plate. It is semi-transparent and looks red due to abundant vascular supply in the nail bed. The more opaque and whitish lunar portion of the nail plate near its root is known as the lunula. The surface of the sin on which the nail rests is known as the nail bed. The fold of the skin, surrounding the lateral and proximal borders of the nail is known as the lateral and posterior nail folds.

SKIN : PHYSIOLOGY

The following are, the functions of the skin:-

1. Protection: It acts as an anatomical barrier from pathogens and damage between the internal and external environment in bodily defense. Langerhan cells in the skin are part of the adaptive immune system.
2. Sensation: Skin contains a variety of nerve endings that react to heat and cold, touch, pressure, vibration and tissue injury.
3. Heat regulation: Skin contains large blood supply which allows precise control of energy loss by radiation, convection and conduction. Dilated blood vessels increase perfusion and heat loss, while constricted vessels greatly reduce cutaneous blood flow and conserve heat.
4. Control of  evaporation : Skin provides a relatively dry and semi-permeable barrier to fluid loss.
5. Storage and synthesis: Skin acts as a storage centre for lipids and water and ergesterol –the provitamin for vitamin D. This ergesterol is irradiated by the ultraviolet light of the sun and converted into vitamin D(calciferol)
6. Absorption: Oxygen, nitrogen and carbon dioxide can diffuse into the epidermis, in small amounts. It can also absorb substances dissolved in fatty solvents like vitamins and hormones. This is the principle behind local application and massaging of various ointment
7. Water resistance: The skin, act as water resistant barriers, so essential nutrients, aren’t washed out of the body.

ECZEMA

Dermatitis and eczema are among the most common dermatological problems accounting for 25-30% of all dermatoses. The terms dermatitis and eczema are synonyms and the two are interchangeable. In the developed world, eczema accounts for a large proportion of skin disease, in both developed and community based populations. It is estimated that 10% of people have some form of eczema at any time, and up to 40% population, will have an episode of eczema during their lifetime.

DEFINITION

The term eczema is derived from the Greek word, “Ekzein”, (Ec means out, and Zeo means boil). It looks as if skin is boiling out. Eczema is defined as an inflammatory disorder or reaction pattern of skin, to external or internal stimuli, characterized by erythema, oedema, vesiculation, oozing, crusting, papules, scaling and lichenification. It is a catarrhal inflammation of a sensitive skin. The Hindustani name is Chambal.

Although eczema and dermatitis are synonymous, Hebra says “Eczema is what looks like eczema”. Dermatitis literally inflammation of skin and denotes all types of cutaneous infections while eczema is a specific type of allergic cutaneous manifestation of antigen-antibody reaction. It is characterized by superficial inflammatory oedema of the epidermis associated with vesicle formation. Hence all eczema is dermatitis, but not all dermatitis is eczema.

PREVALENCE AND INCIDENCE

Eczema can affect people of any age, although the condition is most common in infants and about 85% of people have an onset prior to 5 years of age. Eczema will permanently resolve by age 3 in about half of affected infants. In others, the condition tends to recur throughout life. People with eczema often have a family history of eczema or other allergic conditions such as asthma or hay fever. Up to 20% children and 1-2% are believed to have eczema. Eczema is slightly more common in girls than boys. It occurs in all races. It is not contagious but since it is believed to be partially inherited; it is common to find members of the same family affected. There are proportionately more cases in the summer months while exogenous forms are more frequent in winter. Exogenous forms are low in 5-14 age groups, increasing thereafter in males. Housewife’s dermatitis is common in 20-40 years age group.

STAGES OF ECZEMA

The natural history of eczema is diagrammatically represented as follows:

Erythema

Papules with oedema

Vesicles

Weeping, crusting pustules                                                     Lichenification

Scaling

Healthy skin without scars

The morphoclinical classification into acute, sub acute and chronic stages helps us to decide about the prognosis and line of symptomatic treatment.

1. Acute stage: It is characterized by itchy erythema followed by oedema, papules, vesicles, oozing, crusting and something blisters. Most of the typical eczemas of moderate intensity start with these morphological features. This stage does not last long. In about a couple of weeks, the lesions start to heal. If the cause persists, the eczema may last over months or years to become chronic.
2. Sub acute: This stage shows diffuse erythema, oedema, scabbing and scaling of skin. Acute eczema may pass through this stage before it heals completely or becomes chronic.
3. Chronic: This stage shows moderate erythema, scaling and eventually lichenification. The thick, dark, Asiatic skin has a tendency to early lichenification, if not properly handled.

Clinically, an eczematous disease may start at any stage and evolves into another.

STAGES OF ECZEMA

1. 1. Acute eczema:

Acute eczema blisters

1. 2. Subacute eczema

3.Chronic eczema

Thick lichenified skin

HISTOPATHOLOGY

The histopathological features of eczema reflect a dynamic sequence of changes resulting from inflammation of the epidermis and the underlying dermal structures. These vary with intensity and stage of eczematous process and are frequently modified by secondary events such as trauma and infection.

Epidermal changes

The essential feature is spongiosis, an intercellular oedema that leads to stretching and eventual rupture of the intercellular attachments with the formation of ‘primordial’ vesicles. These commonly occur in discrete foci and in the mid-epidermal region. On the palms and soles, the vesicles do not rupture easily and become large by coalescence. There is a variable infiltration of the epidermis by lymphocytes. Accelerated epidermal activity lead to acanthosis but if spongiosis is intense, disintegration of the suprapapillary epidermis may cause clefts to form, to expose the underlying dermis.

In the sub acute stage, spongiosis diminishes and increasing acanthosis is associated with formation of a parakeratosis horny layer. This often contains layers of dried up serum and pyknotic nuclei of inflammatory cells. Later, the rete ridges become elongated and broadened and hyperkeratosis replaces parakeratosis. The changes are then those of lichenification.

Dermal changes

Vascular dilatation may be the earliest stage and is marked in all stages. The papillary vessels are especially involved and in lichenification may become tortuous. The infiltrate is predominantly lymphocytic, though polymorphs and eosinophils may occur in very acute eczema and eosinophils in particular in eczematous drug eruptions. In the presence of infection, polymorphs may invade the epidermis. In grossly lichenified eczema, prurigo and exfoliative dermatitis, the infiltrate is mixed and maybe done as to stimulate a granuloma.

Complications: The trauma of rubbing or scratching may cause superficial erosions, haemorrhage or subepidermal fibrinoid changes. While some degree of lichenification is always present during a prolonged attack of eczema, it is particularly prominent in atopic dermatitis and has been referred to as ‘neurodermatitis reaction’. At times, extreme hyperkeratosis and papillomatosis develop. With secondary infection, the formation of follicular or subcorneal pustules stimulates the appearance of impetigo, though typical eczematous changes are visible at the edges of the lesion.

Changes in the various stages of eczema

1. 1. Acute: The histological picture is dominated by spongiosis and vesicle formation. The intercellular oedema may be diffuse but more commonly occurs in discrete foci and is most intense in the mid epidermal region. Loosening and disruption of the individual Malphigian cells occur and some intracellular vacuolation maybe found with displacement of nucleus, from the centre of the cell. Loose, shrunken epidermal cells may resemble histiocytes. Vesiculation occurs as a result of further fluid accumulation and detachment of cells. When this is intense, the appearances are those of reticular degeneration. The vesicles and the oedematous epidermis maybe permeated by mononuclear cells, chiefly monocytes.

On the palms and soles, the resistance of the thick stratum corneum delays the rupture of the vesicles, which tend, in consequence to become large and bullous, by coalescence. In the weeping stage, there is thinning or destruction of the suprapapillary epidermis, which may reach the underlying dermis.

1. Sub acute: Spongiosis and Vesiculation diminish and acanthosis increases. A parakeratotic stratum corneum forms, which contains coagulated plasma and the pyknotic nuclei of inflammatory cells. Later, the epidermal thickening becomes more marked and the rete pegs more elongated and broadened. The appearances merge into those of lichenification.
2. Chronic: Hyperkeratosis coexists with areas of parakeratosis. Spongiosis and vesiculation give rise to acanthosis. Cells no longer invade the epidermis but dermal changes become more prominent.
3. Recovery:  In uncomplicated eczema, where no secondary changes or fresh attacks occur, the changes gradually regress to normal. Infection or trauma of rubbing or scratching obviously modifies this process.

Basis of pathological changes

The changes in eczema have been described as a series of chain reactions which take place in the epidermis and proceed from a primordial vesicle to the extrusion, after more or less spongiosis and exocytosis, of a parakeratotic scale. Spongiosis and the presence of primordial vesicle are important in the histological diagnosis of most chronic lesions.

In light and electron microscope studies carried out experimentally, produced allergic contact dermatitis, the earliest changes consist of vasodilatation and extravasations of monocytes from the vessels, followed by spongiosis as they migrate into epidermis. In irritant dermatitis, primary epidermal damage may progress to subepidermal blister formation.

HISTOPATHOLOGY OF ECZEMA

CLASSIFICATION OF ECZEMA

Classification of eczema is not well established owing to a lack of a definitive nomenclature and aetiologies. For practical purposes, eczema has been grossly divided into 2 main groups:exogenous&endogenous. In exogenous eczema, the causative factor is an exogenous one coming from outside the body, whereas in endogenous eczema,the factor is an internal one. The term “endogenous eczema’, has no distinct scientific boundary at present. Basically,endogenous eczemas are those group of eczematous disorders in which the precipitating factors are acting from within the body, and not from outside.However,many eczemas lie within the twilight zone of exogenous and endogenous eczemas. In these cases, both exogenous and endogenous factors simultaneously act as causative factors. Moreover, the same type of eczema may sometimes be provoked by external factors and sometimes by internal ones. Often, both exogenous and endogenous eczemas may be present at the same time in a patient.

ENDOGENOUS ECZEMA	EXOGENOUS ECZEMA
Atopic dermatitis Seborrhoeic dermatitis Asteatotic eczema Nummular eczema Pityriasis alba Stasis dermatitis Lichen simplex chronicus Pompholyx Juvenile plantar dermatosis Autoeczematization	Contact dermatitis Primary irritant dermatitis Allergic contact Infective eczema Physical eczema Photodermatitis Radiational eczema Phytophotodermatitis Eczematous Dermatophytosis 10.  Dermatophytide 11.  Secondary eczematization

ETIOLOGY

Basically, two factors are involved. Firstly, an allergic or a sensitive skin; and, secondly, exposure to an irritant. Darier has correctly said that, “there is no eczema but an eczematous patient”. The general predisposing causes are age, familial predisposition, allergy, debility climate and psychological factors. Eczema usually occurs in infancy, at puberty and at time of menopause. Familial sensitiveness is an important factor. There is usually a personal or family history of allergy i.e. asthma, eczema, hay fever etc. Genetic predisposition is responsible for the preponderance of eczemas in certain families and their absence in others, general physical debility predisposes to eczemas by lowering the resistance of the individual. Climate extremes like heat, dampness and severe cold and also psychological stresses promote the development of eczema. Local factors like xeroderma or ichthyosis, a greasy skin, hyperhidrosis, varicose veins causing congestion and focus of lowered resistance, hypostasis or chilblains predispose to eczema development. In the dry winters of northern India, crackling of the integument of exposed parts may result in eczematization-“eczema crackle”. There is variety of exciting and aggravating factors like chemicals, plants clothes, drugs, diet, trauma etc.

To summarize:

1. Irritants –  Physical, chemical or electrical
2. Sensitizers- Plants,  cosmetics, clothing, medicaments &occupational hazards
3. External infections- streptococci, staphylococci, fungus etc
4. Mental and emotional conflicts, strains and stresses
5. Internal septic focus shedding toxins or causing bacteraemia
6. Diet and state of digestion
7. Diathesis-allergic, xeroderma, hyperhidrotic or seborrhoeic
8. Drugs-given for disease or otherwise
9. State of local or general nutrition
10. Climate-temperature and humidity

VARIETIES OF ECZEMA

1. I. Endogenous eczema

A. Atopic dermatitis

Synonyms: Besnier’s prurigo, infantile eczema, flexural eczema, Asthma-eczema syndrome

Atopic dermatitis (AD) is a classical endogenous eczema. It is a cutaneous expression of the atopic state. Atopy is a genetically determined disorder in which there is an increased susceptibility to form reagin (IgE) antibodies and an increased susceptibility to certain diseases like asthma, hay fever, and atopic dermatitis in which the antibodies may play some role. Atopic dermatitis is a pruritic, recurrent, flexural and symmetric eczematous dermatosis.

History

Atopic dermatitis was first described in 1808, by Robert Wilan. He believed it was a prurigo-like condition associated with pruritus. Later Brocq and Jacquet identified pruritus as the initial event and termed the disease as “neurodermatitis”. They emphasized its neural origin. Besnier observed a familial tendency and association with the clinical features of emphysema, bronchial asthma, hay fever and more rarely gastrointestinal disorders.

In 1925, Coca and Cooke coined the term ‘atopy’, which means ‘out of place’ or ‘strange’ for a group of patients who had a hereditary tendency to develop an urticarial response to food and inhalant substances. Reagin (IgE) antibodies were detected in these ‘atopic’ patients and could be transferred to normal persons by the Prausnitz-Kaustner test. Later Coca and Sulzberger introduced the term ‘atopic dermatitis’ in order to classify the different type of allergic disorders in skin.

Incidence

Atopic dermatitis occurs in between 7&24 individuals per 1000 persons. The highest incidence is seen among children. It now affects 1 in 10 school children. The prevalence of atopic eczema is rising and has increased between 2-5 fold over last 30 years. The proportion of the population capable of manifesting atopic diseases is unknown. Latent atopy can exist, as well shown in identical twins; in only about half do the diseases run a parallel course. An estimated 65% develop atopic dermatitis during their first year of life and 90% develop the condition before the age of 5 years. While rare, atopic dermatitis can begin at puberty or later. While atopic dermatitis resolves in many children by age2, 50% continue to experience signs and symptoms into adulthood-usually as hand eczema. It occurs in all races and skin types.

Aetiopathogenesis

The exact etiology of atopic dermatitis is still unknown. The clinical manifestations depend on various constitutional as well as environmental factors.

a)      Genetic predisposition: Atopic dermatitis has a genetic background. A family history of atopy is obtained in 70% of all cases. If one parent has atopic diathesis, there is a 60% chance of child being atopic. The figure increases to 80%, if both parents are affected .In non atopic clinically normal families, there could be an atopic child. The mode of inheritance appears to be polygenic. Monozygotic twins are often concordant for the disease.

b)      IgE and other immunoglobulin : Raised IgE level is the most consistent immune defect seen in atopic patients. The total IgE is above the normal level (>200 IU/ml) in 80% of atopic dermatitis and is even higher when atopic dermatitis and asthma are simultaneously present. IgE levels above 1000IU/ml maybe found in patients having a very acute phase of the disease. Atopic individuals produce 3-10 times more IgE than normal individuals.

c)      Reduced cell-mediated immunity: A primary-cell defect may be present in atopic patients and even several facts suggest that they have an abnormal cellular immunity. They may develop a severe generalized cutaneous infection like eczema herpeticum, caused by Herpes simplex virus, even when their disease is not active. DNCB sensitization is more difficult in patients having severe atopic dermatitis.

d)     Histamine: The acute inflammation seen in atopic dermatitis maybe due to histamine and other mast cell mediators a basic disorder of cyclic AMP metabolism may lead to increased release of different mediators from the mast cells. As a result, there are high levels of plasma and tissue histamine. Blood eosinophilia is common in atopic dermatitis, leading to liberation of histamine from basophils and mast cells, including pruritus, irritation and lichenification.

e)      Beta-adrenergic Blockade Theory: On beta-adrenergic stimulation, the target cell’s responses of atopic patients are diminished as compared to those of normal persons.

f)       Vascular changes: Vascular changes, white dermographism and delayed blanching of skin are seen in atopic dermatitis. Skin temperature and blood flow is increases up to 6 times, while in chronic dermatitis there is normal blood flow. Central pallor of face is common in adult atopics and is due to vasoconstriction. Acetylcholine injection into normal skin produces red flare but in 70% of atopic patients there is blanching after 3-5 minutes due to increased blood flow and fluid transudation. Increased amounts of acetylcholine are seen in atopic dermatitis patients.

g)      Chemotactic factors: An abnormality of chemotaxis of both polymorphs and monocytes has been detected in atopic dermatitis patients. Small pustules produced by Staphylococcus aureus are seen in such patients and are extremely itchy and immediately excoriated.

h)      Abnormalities in essential fatty acid metabolism: Dry xerotic skin is the most important manifestation of atopic dermatitis. Decreased amounts of ceramides derived from linoleates have been observed in the dry palmar skin of atopic dermatitis patients, associated with increased transepidermal water loss. This water loss is due to reduced sphingolipid, rich in linoleic acid, which has a waterproofing effect. Hansen found reduced levels of unsaturated fat in the blood of atopic children.

i)        Role of foods and aeroallergens: Approximately 10% of foods eliciting a positive skin test can also induce pruritus, with or without erythema, in that patient within 1 hour of an oral challenge. Withholding the foods that showed positive food challenge reactions resulted in a remarkable improvement of atopic dermatitis. Similarly, a positive immediate hypersensitivity skin test can be the initial step in elucidating the aeroallergen triggers of atopic dermatitis. There is a convincing epidemiological association between moderate to severe atopic dermatitis and house dust mites.

j)        Psychological factors: Atopics when under stress tend to scratch and then this habit of scratching may become an automatic reflex. Life stress situations play an important role in triggering the disease and maybe responsible for persistence, exacerbation or relapse. An atopic personality is outwardly calm but seething with suppressed anxieties, frustration, insecurity and aggression, egoistic and possessing above average intelligence. Whitlock believes that the personality is easily influenced, by the presence of the disease, in a very important period of a child’s psychic development. It is also influenced by maternal attitude which varies from lack of affection and inattentiveness to the extreme of rejection. The anger of child consequent to it, finds its outlet in anxiety and hostility, more or less repressed, towards the mother.

Risk factors

a) Family history: A family history of atopic disease such as atopic dermatitis, asthma or hay fever is the strongest risk factor. If 1 or both parents have a history of atopic dermatitis or an allergic condition, the child is much more likely to develop atopic dermatitis.

b) Location: Living in a developed country, urban area or northerly part of the world increase the risk.

c) Age: Appears before 1 year of age in 65% of people and 90% develop it before reaching 5 years of age. Teething is another factor in young children.

d) Gender: Females are slightly more likely to develop it than males.

e) Maternal age during delivery time: Atopic dermatitis tends to be more common when the mother gives birth to a child later in her childbearing years

f) Year born: During the last 40 years, a steadily increasing number of people worldwide, mostly children have developed atopic dermatitis. In the Unites states alone, the prevalence of atopic dermatitis in children born after 1980 increased by 15-20%. This equals a 3-4 fold increase over 5% prevalence rate reported during the 1950s in school age children.

g) Social class: Atopic dermatitis tends to be more common in higher social classes.

h) Family size: Atopic dermatitis tends to be more common in immediate families that are smaller in size.

Histopathology

The histological features are usually suggestive of chronic dermatitis. In infancy, early lesions show acanthosis with a varying degree of spongiosis, oedema of the dermis and infiltration with lymphocytes, histiocytes, plasma cells and eosinophils, sometimes in large numbers. Rarely marked spongiosis with intraepidermal, microvesiculation suggestive of sub acute dermatitis is seen in oozing areas. New spongiotic areas, exocytosis of mononuclear cells and parakeratosis are found. Rete ridges are regularly elongated in long standing cases. Electron microscopic examination shows an increased number of lysosomes within the keratinocytes, in areas of parakeratosis. In later age groups, the histology is that of lichenification, sometimes with rather more eosinophils in the dermis than are found in the lichen simplex.

Clinical features

Itch is the cardinal symptom of atopic dermatitis. All the grossly visible signs, inflammation, lichenification and excoriations are sequential and secondary. In atopic dermatitis, the eruption is not itchy but it is the itchiness that is eruptive. Atopics have xerotic, itchy skin, with a low threshold for itching. Sweating, friction, contact with wool, trauma, temperature changes and psychic stress can set up a bout of scratching. An itch-scratch-itch cycle is easily establishes. The scratching is largely responsible for the clinical feature. The histopathological changes too are largely caused by rubbing and scratching.

Atopic dermatitis has a chronic fluctuating course with the morphology and distribution of lesions varying with the age of the patient. Another cardinal feature is xerotic skin. The lesions of atopic dermatitis are papules, papulovesicles and oozing, lichenification and excoriation.

The disease is conveniently divided into, the following phases in its evolution, as the child grows:

a)      Infantile phase: Lesions first appear, after the second or third month. Cases having an early onset, even during second or third week are also seen. Redness and scaling appear on the scalp around the cradle cap and soon spread to cheeks, and later involve the trunk and extremities. When the infant begins to crawl, the exposed surfaces particularly, the extensor aspects of knees are involved. Groups of itchy red papules erupt and weep. The child maybe too young to scratch, but will rub its head and face on pillow. The eruption may spread to napkin areas and retro auricular areas. Because of the discomfort, the child does not sleep and will keep the parents awake by crying. In severe cases, almost the whole body surface is involved and the child tears at its skin in frenzy, drawing blood with its finger nails. Later the papulovesicles may become exudative and crusted. In majority, the disease heals by the age of 2, while others progress to childhood phase.

b)      Childhood phase: As the infant grow, the distribution of the lesions changes. Involvement of the antecubital and popliteal fossa begins at about 18 months. Other sites affected are sides of the neck, and ankles. The face is less frequently involved. The lesions are dry papules and less acute; gradually the characteristic lichenification appears. Exudative lesions occur in hands and wrists but later the skin is dry and lichenified. In some children, disease has an extensor distribution. Severe pruritus produces intense scratching and a restless, anxious and hyperactive child. Lip/perioral involvement, seen as scaling or fissuring may occur.

c)      Adult phase: In this phase lichenification is the dominant feature particularly in the flexures. Lesions may also be present on neck, upper limbs and sometimes the face. The clinical feature is of dry slightly elevated papules that tend to coalesce to form lichenified slightly scaly plaques. Excessive scratching may cause excoriations, oozing, crusting and secondary infection. The skin becomes thick, rough and has a leathery quality. Nipple dermatitis is an infrequent sign of atopic dermatitis in young women. Hand involvement maybe the first and only sign of atopic dermatitis in young mothers. In young adults, psychological factors may aggravate the disease. Patients older than 45 years of age constitute 2% of the cases. In the majority of those with persistent disease, psychological factors play an important role. Some patients may develop pruritus ani, scrota or vulvae.

Features specific for atopic dermatitis

1. White dermographism: In normal people, firm stroking of the skin results in a red line, while in atopics, the line is first red and then becomes white. It may occur in other dermatoses and is thought to be due to local accumulation of fluid causing oedema, which obscures the colour of the underlying vasculature.
2. Central pallor of the face: It is common in adult atopics and is believed to be due to vasoconstriction
3. Cheilitis
4. Conjunctivitis
5. Icthyosis –fish skin appearance
6. It can be congenital/acquired
7. Exfoliative dermatitis
8. Follicular hyperkeratosis or keratosis filaris
9. Hyper linear palms and soles

Associated disorders and complications

1. Xerosis: Dry skin/xerosis is a hallmark of atopic dermatitis. It usually worsens during periods of low humidity, as in winter. Dryness of skin gives rise to pruritus. The xerotic skin of an atopic dermatitis patient has a reduced water binding capacity and a high transepidermal water loss.
2. Ichthyosis vulgaris: Seen in 20% of cases. Mainly seen on legs and abdomen.
3. Keratosis pilaris: Asymptomatic hyperkeratotic follicular papules are frequently noticed on the extensor surfaces of the upper arms and anterior thighs in atopic patients. It worsens in winter and partly heals in summer.
4. Pityriasis alba: Seen in both normal children and those with atopic dermatitis.
5. Hyperlinear palms and soles: These are often seen in atopic dermatitis patients.
6. The Dennie-Morgan fold: It is a double line seen under the lower eyelid of patients with atopic dermatitis. It may be present at birth or may appear soon after. It gradually disappears with advancement of age. Atleast one fold on the lower eyelid has to extend beyond a vertical line passing through the pupil to be called a Dennie-Morgan fold.
7. Lichen spinulosus: The lesions are characteristic grouped hyperkeratotic follicular spines arranged in occasionally pruritic patches on the trunk. It is commonly seen in black skin. Sometimes the lesions are hypopigmented.
8. Ocular changes: These include periorbital dermatitis, allergic and vernal conjunctivitis, cataract and keratoconis. Periorbital dermatitis may vary from mild xerosis and scaly lesions, to severe lichenification of the eyelids and even ectropion. Itching and rubbing may result in madarosis. Conjunctival allergy initiates persistent rubbing of the eyes, which may lead to periorbital dermatitis. The palpaberael mucosa maybe covered with small cobblestone-like masses; due to infiltration of inflammatory cells in the vernal conjunctiva.21% of severe atopic dermatitis patients have posterior and anterior cataracts. Prompt control of severe dermatitis of the face is very important for prevention of atopic cataracts.  A cone-shaped cornea or keratoconus may be seen in the second or third decade in very severe cases of atopic dermatitis and may require correction by corneal transplantation. Rarely retinal detachment maybe associated with keratoconus.

Complications

Increased susceptibility to infection is seen in atopic dermatitis, particularly in children who are more prone to develop viral and bacterial skin infections. The viral infections are caused by herpes and vaccinia virus and known as eczema herpeticum and eczema vaccinatum respectively. These eruptions are called Kaposi’s varicelliform eruptions. Eczema vaccinatum previously used to occur when children or their family members were vaccinated for smallpox, but is no longer seen. Herpes is often transmitted from a close family member who has herpes labialis or any other herpetic lesions. A history of exposure is not always present. The child may develop fever and vesicular lesions on the eczematous skin which readily cause small erosions and crusts. Later on, the rash may extend to normal skin.

Atopic dermatitis patients are more susceptible to develop verrucae and molluscum contagiosum and dermatophyte infection.

Diagnosis

Diagnosis is entirely clinical. It is based on the distribution of lesions, their duration and often a family history of atopic disorders. Atopy is characterized by high serum IgE levels or high specific IgE levels to certain ingested or inhaled antigens. The latter can be tested by radio-immunoabsorbent assay tests (RAST) of blood, or indirectly by skin pricking test. A peripheral blood eosinophilia may also be seen.

Criteria for diagnosis of atopic dermatitis

Major features

1. Pruritus
2. Typical facial morphology and distribution

a)      Facial and extensor involvement in infants and children

b)      Flexural lichenification in adults

1. Dermatitis chronic or chronically relapsing
2. Personal or family history of atopy, asthma, allergic rhinitis or atopic dermatitis

Minor features

1. Cataracts
2. Cheilitis
3. Conjunctivitis, recurrent
4. Eczema, perifollicular accentuation
5. Facial pallor/erythema
6. Food intolerance
7. Hand dermatitis; non allergic; irritant
8. Ichthyosis
9. Elevated levels of IgE

10.  Immediate (type I) skin test reactivity

11.  Infections

12.  Itching when sweating

13.  Keratoconus, keratosis pilaris

14.  Nipple dermatitis, orbital darkening, palmar hyperlinearity, Pityriasis alba, white dermographism, wool intolerance, xerosis

Differential diagnosis

1. Scabies: A recent history of itching in other family members towards scabies. Dryness of skin is a feature of atopic dermatitis. Facial involvement rules out scabies, although infants and children with eczematized scabies may develop an eczematous rash on the face mimicking that due to atopic dermatitis. In such infants, scabetic involvement of palms and soles, if present is characteristic. Typical burrows may occasionally be found in scabies. Demonstration of mites is the definitive proof.
2. Seborrhoeic dermatitis: It usually begins around age of 6 weeks and is asymptomatic. Scalp and intertriginous areas are mainly involved, showing yellow greasy scales on the erythematous base.
3. Contact dermatitis: it is uncommon in infants and young children and diagnosed by a well demarcated distribution corresponding to the application of the irritating agent
4. Ichthyosis vulgaris: it is often associated with atopic dermatitis. Scaling without erythema or itching denotes Ichthyosis.
5. Psoriasis: uncommon in younger age groups. Asymptomatic with well defined erythematous plaques with loose silvery scales. Auspitz sign is positive. Common areas of involvement are scalp, elbows and knees. In infants, the commonest site is the diaper area.
6. Dermatophytosis: Erythema, scaling and vesicles around a spreading border with central clearing, suggest the diagnosis of dermatophyte infection, which is rarely seen under the age of 10 years. 10% potassium hydroxide slide preparation when examined under microscope shows hyphae.
7. Neoplastic disease: The neoplastic diseases, Letterrer- Siwe disease and histiocytosis X in children and mycosis fungoides and Sezary syndrome in adults, has eczematous plaques that become haemorrhagic or indurated.
8. Other diseases:

The following diseases may manifest eczematous lesions:

a)      Acrodermatitis enteropathica

b)      Agmmaglobulinaemia

c)      Ahisidinaemia

d)     Ataxia-telengiectasia

e)      Gluten sensitive enteropathy

f)       Hartnup’s disease

g)      Hurler’s syndrome

h)      Leiner’s disease

i)        Phenylketonuria

j)        Wiskott-Aldrich syndrome

Prognosis

In many patients, the disease heals after the infantile phase. After the second decade, there is a tendency to spontaneous healing. Improvement around puberty is common. Elderly patients have atopic dermatitis rarely. 30-50% infantile patients may develop asthma or hay fever later. High total cord IgE levels have a predictive value for the development of atopic disease. Elevated phosphodiesterase levels at birth also have a predictive value. Unfavourable prognostic factors are:

1. Persistent dry or itchy skin in adult life
2. Widespread dermatitis in childhood
3. Associated allergic rhinitis
4. Family history of atopic dermatitis
5. Associated bronchial asthma
6. Early age of onset
7. Female sex

ATOPIC DERMATITIS

Typical atopic eczema                 A patch of eczema that has been scratched

The occurrence and evolution of atopic eczema in different age groups

Atopic dermatitis of back      Atopic dermatitis in hands            Atopic dermatitis on the back of  knee

Eczema in flexural folds                         Perioral eczema                                    Severe eczema around eyelids

Atopic dermatitis in cheeks&neck                      Erythematous plaques characteristic of atopic dermatitis

Chronic atopic eczema                                 Lichenification in chronic eczema

AD superinfected with Staphylococcus aureus . AD cause hypopigmentation, as seen on the arms of the patient

Rash seen as scaly bumps over each hair follicle                        Atopy patch test

INFANTILE ECZEMA

ATOPIC DERMATITIS IN CHILDHOOD

B. Seborrhoeic dermatitis

Synonyms: seborrhoeic eczema, cradle cap (in infants0-6 months), dandruff, seborrhoea

The term “seborrhoea” designates increased and altered secretions of the sebaceous glands resulting in excessive oiliness of the skin. It is very common in tropical climates. Many adults have an oily complexion, the so called seborrhoeic diathesis.

Definition

Seborrhoeic dermatitis is a common, chronic inflammatory dermatoses having a distinct distribution in areas of greatest sebaceous activity.

Unna first devised the term “seborrhoeic eczema”. Brocq suggested “seborrhoeide” and Darier, elaborated the concept of ‘ide’ reactions to a primary focus and preferred the term “eczematide”. In France, certain forms of seborrhoeic dermatitis are still commonly designated eczematides, but for others Brocq’s term ‘parakeratoses’ is preferred.

Incidence

It develops in all races. Tends to begin during infancy (newborn -6 months), puberty or between 40&70 years of age. After 6 months of age, the condition rarely appears before puberty. When seborrhoeic dermatitis begins during infancy, it usually clears by 9-12 months of age. At all ages, it is more common in males than females.

Aetiopathogenesis

The exact cause of seborrhoeic dermatitis is unknown. The yeast Pityrosporum ovale is probably a causative factor but both genetic and environmental factors influence and contributes to the onset and cause of the disease process. The yeast P.ovale, various bacteria and, in infants Candida albicans are found in increased numbers within the lesions, although it is not known whether their role is primary/secondary. Although normal persons harbor P.ovale, an increase in the number of yeast correlates well with the disease activity.

It has also been emphasized that seborrhoeic dermatitis is a hyperproliferative disorder in which effective therapeutic agents act by a cystostatic mechanism. Seborrhoea, perspiration and emotional stress are additional factors in aetiopathogenesis. Hypothalamic-controlled sebotrophic hormones may act as sebum regulators by means of the peripheral nerves and sebaceous gland enzymes, including lesions of the seborrhoeic dermatitis.

Another possible contributory factor may be a disorder in the dopaminergic pathways. It is seen in neurological disorders like Parkinsonism, Idiopathic post-encephalitis and drug induced Parkinsonism. There is an increased rate of sebum excretion and treatment with L-dopa causes a reduction of the same.

Autoimmunity to epidermal scales, or food allergy especially in infants, may cause the disease. Perianal localization of the disease suggests the possibility of autoimmunity, to Candida albicans, with a psoriasiform id, although potassium hydroxide preparations are negative.

Sebaceous gland dysfunction maybe an important contributory factors, as disease activity depends on the course of sebaceous gland activity. The sites of predilection, at least in adults, produce the maximum amount of sebum and contain the highest amount of surface fats. There are an increased proportion of cholesterol triglycerides and paraffin and a corresponding decrease in squalene, free fatty acids and wax esters in the surface of seborrhoeic dermatitis patients.

Hormonal factors may trigger seborrhoeic dermatitis, since the disease usually starts at puberty. Menstrual cycle causes a change in the sebaceous gland activity and maternal hormones have a direct influence on the disease activity in infants. Seborrhoeic dermatitis of infancy spontaneously disappears with cessation of maternal androgen stimulation.

Other presumed etiological factors are increased sugar consumption, vitamin B including B₁₂ malutilization, Biotin deficiency, food allergy (in infantile seborrhoeic dermatitis) and relatively low humidity in winter.

Risk factors

1. Family history of eczema
2. Oily skin/hair
3. Stress
4. Fatigue
5. Cold, dry climate
6. Gender: males tend to develop more often and have more severe cases
7. Obesity
8. Injury to skin, such as an abrasion or scratch
9. Lotions or other topical that contain alcohol
10. Having acne rosacea, psoriasis or blepharitis
11. Parkinson’s disease, HIV and recovering from stroke or heart attack increase the risk significantly. 90% of HIV infected individuals develop seborrhoeic dermatitis.
12. Medications, including interferon-a, lithium and psoralen increases the risk.

Clinical features

The seborrhoeic state: It is purely a clinical concept. The skin of the face appears greasy and is often pale. The follicular orifices are patulous and conspicuous and the skin feels slightly thickened. They commonly originate in the hairy skin and involve scalp, face, on &behind ears, presternal and interscapular regions and flexures and around umbilicus. The lesions tend to be dull or yellowish red sharply marginated and covered with greasy scales.

Infants

During infancy, seborrhoeic dermatitis usually begins within the first few days or weeks of life, commonly between 3-8 weeks as greasy scaling in the scalp called cradle cap. Small round or oval, erythematous scaly lesions are seen on the face and the napkin area. Well-defined erythematous scaly lesions which rapidly become confluent appear in the diaper area, face, forehead, eyebrows, eyelids and nasolabial folds. The retroauricular area and temples are also affected. The scales are large, yellowish and greasy on the scalp but smaller elsewhere. There is hardly any itching. Infant is well. Feeding and sleep are undisturbed. Prognosis is good and most cases clear by the age of 3-4 weeks. In a few, it may take 2 months or longer.

Adults

a) Scalp: Dandruff denotes an exaggerated loss of keratinized cells from the scalp surface. Itchy dandruff maybe a manifestation. Later, perifollicular erythema and scaling from well-defined patches which coalesce and cover the scalp to extend beyond the forehead hairline as the ‘corona seborrhoeica’. There may be reversible hair loss. Behind the ears, there is erythematous greasy scaling and a crusted fissure may develop in the retroauricular fold. The lesions may involve the adjacent scalp. In the external ear, there may also be itchy scaly lesions due to otitis externa.

b) Face: Areas of erythema and scaling involve the nasolabial folds. Blepharitis is seen as a red eyelid margin covered by small scales. Later, small ulcers form, covered with crusts, leading to destruction of eyelash hair. The beard area in men is involved and lesions are similar to those in scalp. They tend to be more follicular and show more pustulation.

c) Trunk: The interscapular and presternal areas show small brown follicular papules covered by a greasy scale. Extension and coalescence of these lesions produce circinate patterns-the petaloid form. Less common is the Pityriasis form.

d) Flexures: Seborrhoeic dermatitis is seen as diffuse well-marginated erythema with greasy scaling and a fissure covered with crusts. Later exudating dermatitis may spread around the fold. Secondary bacterial and Candidal infection is quite common.

Seborrhoeic intertrigo: Moist red intertrigo of body clefts, the submammary areas, groins, umbilicus and axillae may occur in association with widespread seborrhoeic lesions or alone.

Differential diagnosis

Atopic dermatitis, psoriasis, tinea capitis (differentiated by mycological examination), in the Letterer-Siewe disease, petechial, crusted, erosive, scarring as well as seborrhoeic lesions, usually affecting the creases are present. Leiner’s disease, secondary to c₅ dysfunction, may manifest clinically as severe seborrhoeic exfoliative erythroderma. Intractable diarrhea and recurrent infections are associated.

Sebopsoriasis (seborrhoeic psoriasis/seborrhoeiasis)

It signifies a bridge between psoriasis and seborrhoeic dermatitis, since features of both diseases are present simultaneously. Patients present with a scaly, psoriasiform dermatitis in the scalp and lesions elsewhere on the body and face with a greasy appearance. This suggests a seborrhoeic tendency manifesting itself in a subject genetically predisposed to psoriasis. Occasionally, the diaper area maybe involved with a psoriasiform eruption termed as napkin dermatitis. Nail pitting maybe absent. Such patients require long term follow-up.

Pityrosporum folliculitis

Synonym: seborrhoeic folliculitis

Definition: This is a follicular infection caused by the yeast Pityrosporum ovale.

Etiology: Pityrosporum yeast is present in large numbers within the follicles and blocks the ostium by producing scales. They also break down triglycerides by hydrolysis and liberate free fatty acids, resulting in folliculitis. They may also trigger off the inflammatory process by alternative complement pathway.

Clinical features

Dome shaped follicular papules, 2-4 mm in diameter, are seen along with small pustules. The sites of the predilection are upper back, shoulders and chest. Lesions on the forearm, lower legs or even the face are common. They may itch occasionally.

Differential diagnosis: closely resembles acne, but differentiated by pruritus and absence of comedones.

Diagnosis

Pityrosporum yeast can be identified by skin scrapings.

SEBORRHOEIC DERMATITIS

Seborrhoeic dermatitis involving scalp

Seborrheic dermatitis affecting the forehead ,in &around ears, chest

Sebopsoriasis                                                        Pityrosporum folliculitis

1. C. Asteatotic eczema

Synonyms: Eczema hiemalis, eczema craquele, xerotic eczema, winter eczema/winter itch, senile eczema

Definition

Asteatotic eczema is an eczematous dermatitis, occurring particularly on legs, arms and hands in which a dry, cracked, fissured skin is a predominant feature and which is more marked in the winter and in the elderly.

Histopathology

Features of mild, subacute eczema, with a varying amount of dermal infiltrate, is seen.

Clinical features

It is more common in aged skin and is frequently seen in young children. Sometimes it may be associated with atopic dermatitis and ichthyosis. The ailment is aggravated by cold, dry weather particularly in those who bathe frequently and for prolonged periods.

The asteatotic skin is dry and slightly scaly. The surface of the back of the hands is marked in a criss-cross fashion, as though the continuity and flexibility of the keratin had been disturbed. The finger pulps are dry and cracked, producing distorted prints and retaining a prolonged depression after pressure (parchment pulps). On the legs, the pattern of superficial markings is more marked and deeper (crazy-paving pattern). In some patients, the fissures may become haemorrhagic. The borders become erythematous, slightly raised and frank eczematous changes may develop. Similarly, on the hands, localized areas become ‘chapped’ or itchy and eventually form eczematous patches.

The condition can remain in this state for months relapsing each winter and clearing in the summer, but eventually becomes permanent. Scratching, rubbing or contact irritants and sensitizers cause further eczematous change or spread or a more diffuse vesiculosquamous eruption occurs. Nummular eczema can also occur in this background. Irritation in this form of eczema is often intense and worse with changes of temperature, particularly on undressing at night.

ASTEATOTIC ECZEMA

1. D. Nummular eczema

Synonym: Discoid eczema

Definition

It is a common pattern of cutaneous reaction characterized by acute eruptions appearing as minute ‘pin-point’ vesicles and papules that may enlarge by confluence or peripheral extension to form characteristic, discrete, erythematous, coin-shaped patches.

Incidence

Men develop it more frequently and tend to have their first outbreak between 55 and 65 years of age. Another peak period for developing nummular dermatitis is between the ages of 15&25 years. Women are more likely to develop the condition. It is rare in children.

Etiology

The exact etiology is unknown. Probable factors are bacteria, hypersensitivity and xerotic skin. Aggravating factors are soap, frequent bathing, wool, topical medicaments, emotional stress and alcohol. Some patients show sensitivity to:

1. Mercury:  Exposure to mercury, a component of dental fillings can cause nummular dermatitis. Even handling the materials in a dental office or lab can cause outbreak by inhaling the mercury vapour.
2. Rubber, nickel, formaldehyde or neomycin: If the patient is allergic to any of these, the skin will clear only when the substance is avoided.

Risk factors

1. Medical condition: A history of xerosis or atopic or stasis dermatitis increases the risk, as does having poor blood flow and swelling in the legs.
2. Environment: A low humidity seems to increase the risk and also worsen existing nummular dermatitis.
3. Injury to the skin: An insect bite, contact with chemicals, or an abrasion may trigger an outbreak.
4. Bacterial skin infection
5. Certain medications: Medications like otretinoin. Some patients who are treated for hepatitis C with interferon develop severe, generalized nummular dermatitis.

Histopathology

Features of subacute dermatitis are usually seen. Epidermal changes include extensive parakeratosis, moderate acanthosis, scattered intraepidermal vesicles surrounded by spongiosis at various levels and lymphocytic exostosis. Intercellular oedema is an important hallmark. Electron microscopy reveals features resembling allergic contact dermatitis.

Clinical features

The condition usually starts on the back of the hands, extensor surfaces of the arms, legs, thighs, shoulders, buttocks, breasts or nipples. The lesions are discrete, coin shaped, erythematous, oedematous, vesicular and crusted patches, o.5 to 5cm or larger in diameter. Koebner’s phenomenon may be associated. In some cases, a lesion may be more extensive leading to a palm-sized or larger patches from which exudation may occur. Pruritus is usually severe and may have a paroxysmal, compulsive quality and nocturnal timing as seen in circumscribed neurodermatitis. Hence, sometimes referred, to as nummular neurodermatitis.

All forms of nummular eczema are chronic, with partial remissions during which the plaques tend to heal first in their centres. Most forms tend to relapse at long or short intervals and most are worst in the colder months of the year. The prognosis in the individual case must be based on a careful assessment of all possible contributory factors and in general, less favourable in older patients.

Differential diagnosis

1. Tinea/ringworm : Elements of the plaque of nummular eczema are not follicular and vesiculation occurs throughout the plaque and is not confined to its advancing margin. Scraping of margin shows mycelium in tinea.
2. Exogenous contact dermatitis: It should be suspected, if the patches are few, asymmetrical or of unusual configuration.
3. Psoriasis: Lesions are dry with no irritation. In parapsoriasis, finely scaling plaques commonly occur on trunk/thighs.
4. Exudative discoid lichen dermatitis: The patient is usually middle aged Jew. The lesions are intensely irritable and involve scrotum, penis, trunk and limbs.

NUMMULAR ECZEMA

1. E. Pityriasis alba

Definition

This is a non specific dermatitis showing erythematous scaly patches which after healing produce residual depigmentation.

Incidence

It occurs predominantly in children between the ages of 3&16, in which the incidence may reach up to 30-40%. The sexes are equally susceptible.

Etiology

The exact etiology is unknown. It is not directly caused by an infectious agent. Although commonly associated with atopic dermatitis, its occurrence is not infrequent in non atopics. Precipitating causes are wind, soap and sunshine.

Histopathology

Histopathological features are non specific. Hyperkeratosis, parakeratosis, moderately dilated blood vessels in the upper dermis; mild perivascular infiltration and oedema of the papillary dermis are seen. Pigment is decreased or reduced in the basal layer. The lack of pigmentation, maybe due to, ultraviolet screening effect of the thickened horny layer, and reduced capacity of hypermetabolic epidermal cells, to receive granules. On electron microscopy of involved skin, the number of active melanocytes is seen to be reduced and the number and size of melanosomes decreased.

Clinical features

This dermatosis commonly occurs before puberty. The most common sites of involvement are face, neck and arms. At the onset, a non specific erythema is visible, which later turns into a scaly patch and finally a hypopigmented area results. The hypopigmentation is not permanent. The lesions are usually symptomless, but some patients feel mild pruritus. Lesions are usually stable. The individual lesion is a round, oval or irregular plaque, red, pink or skin coloured with fine lamellar or branny scaling. The hypopigmented patches are usually multiple. Size is usually 0.5-2cm in diameter, but maybe larger on trunk. Most cases persist for some months and some may still show leucoderma for a year on more, after all scaling subsides. Recurrent crops of new lesions may develop at intervals. The lesions may fade with the advancement of age, although some cases may persist even in adulthood.

Diagnosis

The age incidence, fine scaling and distribution of the lesions usually suggest the diagnosis.

Differential diagnosis

The condition is often confused with Pityriasis versicolor, early vitiligo and leprosy. Lesions of vitiligo and leprosy don’t have scales. A potassium hydroxide slide preparation reveals that the fungi in Pityriasis versicolor. A histamine test, sweat function test or histopathology maybe required to confirm leprosy.

PITYRIASIS ALBA

1. F. Stasis dermatitis

Synonyms: Gravitational dermatitis, venous eczema, venous stasis dermatitis, varicose eczema

Definition

This type of eczema occur secondary to chronic venous insufficiency.

Incidence

It typically develops in middle aged or older people, due to poor circulation. It rarely occurs before the age of 40 years. Females are more likely than males to develop condition.

Aetiopathogenesis

Chronic venous insufficiency is a pathologic condition of the lower extremity that results from stasis of venous blood flow. It maybe localized or may involve the entire extremity. It commonly follows an old ileofemoral thrombophlebitis which produces thickened inelastic vein walls with damaged incompetent valves and partially or sometimes completely obstructed lumina. Varicose veins of primary type, especially long standing are a common cause of less severe chronic venous insufficiency. Other causative factors are obstruction of one of the main veins of the extremity, particularly the ileofemoral, due to external pressure, neoplastic invasion, extensive haemangiomas, congenital or acquired arteriovenous fistulas and congenital absence of valves.

Venous flow against gravity in the lower limbs is made possible, physiologically, by the action of the calf muscles and competent valves in the veins. Muscular compression of elastic veins forces blood upwards while the valves prevent retrograde flow. This vital pump mechanism is called peripheral venous heart. It fails most often in chronic venous insufficiency because of extensive damage to the veins from thrombophlebitis or from structural weakness in varicose veins.

Chronic venous insufficiency leads in sequence to venous hypertension, excess fluid loss through dilated capillaries and inadequate oxygen and metabolite exchange in tissues. Stasis leads to hypoxia and poor nutrition of tissues and this result in dermatitis.

Irritant and allergic contact dermatitis often complicates stasis dermatitis. Increased numbers of HLA-DR positive cells and Langerhan cells stained with ATPase are supportive evidence for the role of contact allergy in stasis dermatitis.

Risk factors

1. 1. Varicose veins
2. 2. Deep vein thrombosis
3. 3. High B.P
4. 4. Sedentary lifestyle
5. 5. Obesity
6. 6. Heart disease such as congestive cardiac failure
7. 7. Kidney failure

Pathology

Doppler velocity measurement confirms the presence of venous insufficiency. Arterial studies can be similarly performed to exclude ischaemic vascular disease. The histopathology of stasis dermatitis is nonspecific and usually shows features of subacute or chronic dermatitis. A considerable amount of hemosiderin is seen throughout the dermis. Old lesions show numerous old capillaries embedded in fibrotic dermis.

Clinical features

Stasis dermatitis can begin so slowly that it is barely noticeable or so rapidly that it seems to develop overnight. The first clinical manifestation of chronic venous insufficiency is usually oedema. Swelling occurs in one or both lower legs. In severe cases, the swelling can include and extend to just beneath the knee. When the oedema has been present for some time, irregular patchy areas of brown pigmentation (due to haemosiderin deposition) may appear, mostly above the ankle. Melanin may also be deposited in the skin as a result of scratching or irritation. Purpura and petechiae are occasionally present. Open sores are painful and heal slowly.

Stasis eczema can be of chronic scaling type and severe itching and irritation maybe present. Patches of skin can be dry and scaly or ooze. Honey coloured crusting occurs when the skin becomes infected. Skin thickens and darkens with repeated scratching and rubbing. Violet coloured lesions may appear on lower legs and dorsum of feet. It is manly in areas of marked congestion of the skin or near stasis ulcers or scars of healed ulcers. Skin on affected areas, have a susceptibility, to contact allergy.

Diagnosis

It begins with a complete medical history and visual examination of the skin. Blood tests, Doppler testing to evaluate blood flow to legs, patch test and biopsy of affected skin are done to confirm diagnosis.

STASIS DERMATITIS

G. Lichen simplex chronicus

Synonyms: Lichen simplex, circumscribed or localized neurodermatitis, Nodular prurigo

Definition

It is a common, chronic usually solitary plaque of thickened skin occurring due to repeated rubbing, scratching or both.

Incidence

It occurs in mid to late adulthood, with most cases developing between 30 and 50 years of age. It is rare before adolescence and is more common in females. It is more common in Asians, black Africans and Oriental patients

Etiology

Exact cause unknown and usually occurs in atopic individuals.

Risk factors

1. 1. Tight clothing made of synthetic fabric or wool
2. 2. Dry skin
3. 3. Long-term exposure to traffic
4. 4. Exposure to allergens and skin irritants e.g.: People using hair dye containing P-Phenylenediamine(PPD) may develop neurodermatitis
5. 5. Heat
6. 6. Insect bite
7. 7. Period of intense stress or emotional trauma
8. 8. Poor blood flow
9. 9. Scar especially a keloid type scar

Histopathology

Histologically, features suggestive of chronic dermatitis are observed. Hyperkeratosis with focal areas of parakeratosis, acanthosis with rather regular elongation and broadening of papillae are seen. Apart from a chronic inflammatory infiltrate, the dermis often shows a fair number of fibroblasts and some fibrosis even in the papillae and papillary dermis.

Clinical features

It usually presents as a solitary lesion although some patients have multiple lesions and tend to be fairly well circumscribed but don’t have sharp margin. It appears thickened, scaly and hyperpigmented areas of lichenification. It starts with intense itching that becomes tender with increased rubbing or scratching. The surface is often associated with no vesiculation or weeping. Common sites are the nape of the neck, lateral calves, upper thighs, upper back, scrotum or vulva although any area can be affected.

Nodular prurigo is a different pattern of cutaneous response to scratching, rubbing or pricking. It is a chronic unremitting condition, often resistant to treatment. Individual, itchy papules and domed nodules appear on the trunk and extensor surfaces of the limbs. They show significant surface damage from scratching. These two conditions overlap in some patients showing mixed feature. Atopic individuals are predisposed to develop these conditions. In the elderly, nodular prurigo, maybe an early sign, of bullous pemphigoid, before the more typical, blistering phase has appeared.

LICHEN SIMPLEX CHRONICUS

H. Pompholyx

Synonyms: Dyshidrosis, dyshydrotic eczema, cheiropompholyx, hand eczema, vesicular palmoplantar eczema

Definition

It is an acute recurrent or chronic idiopathic pruritic non-inflammatory vesicular eruption (Pompholyx-bubble) of the palms and sides of fingers (cheiropompholyx) or soles (pedopompholyx).

Incidence

Most frequently begins between 20&40 years of age, but develop earlier or later. Rare in children but can develop in children with atopic dermatitis. It occurs in all races.

Etiology

Dyshidrosis is incorrectly linked as an abnormality of swelling. Exact cause is obscure. Monozygotic twins maybe involved simultaneously suggesting a genetic role. Although areas affected by disease correspond to those of emotionally activated palmoplantar sweating, hyperhidrosis is not a constant feature. Serial sections of pompholyx vesicles have revealed that sweat ducts are often pushed aside by the tense vesicular fluid, which suggest, that vesicles cause the rupture of sweat gland. A family history of atopy has been found in 54 out of 131 patients. Occasionally, along with Pompholyx, active Dermatophytosis is seen elsewhere in the body. Irritant or allergic dermatitis resulting, from the treatment of tinea pedis, may also, precipitate palmar pompholyx. The role of ingested material e.g.: nickel, chromate or cobalt has been alleged .Potential allergens such as perfumes, fragrances’ and balsam of pern maybe contributing factors. Drug eruptions, bacterial foci and material stress have been rarely implicated in pathogenesis.

Risk factors

1. 1. Stress: Most common risk factor. Many patients report a stressful period before an outbreak.
2. 2. Gender: Females tend to develop dyshydrotic eczema more frequently than males.
3. 3. Weather: Flare ups are most frequent in hot, humid weather.
4. 4. Preexisting atopic conditions: e.g. atopic eczema, hay fever or asthma
5. 5. Preexisting contact dermatitis: It increases the risk.
6. 6. Preexisting infection: Having infection in another body part increase the risk. One-third of dyshydrotic eczema patients had their hands clear, after they received treatment of athlete’s foot.
7. 7. Metal implant: such as hip replacement. There’s a direct correlation between a metal allergy and developing dyshydrotic eczema.
8. 8. Aspirin, OCP and smoking: It increases the risk.

Clinical features

Groups of clear vesicles, which appear deep seated and sago-like and pustules, involve the lateral aspect of fingers, palms and soles, usually symmetrically. There is no erythema, but a sensation of heat and vasodilatation of palms may precede attacks. Absence of erythema is a diagnostic point in early stage. The lesions are tiny (2-3mm), frequently light brown in colour and often evolve into crusts. At times, the vesicles may coalesce to form bullae, especially on feet. The attacks, subsides spontaneously and resolution occurs within 10-14 days, leaving behind slight scaling. The course of the disease is chronic with recurrent episodes of vesiculation. Lesions are very itchy. Bacterial superinfection may lead to pustulation. Hyperhidrosis is common. Emotional stress often precipitates vesiculation. At times it takes a dry and hyperkeratotic form from the very beginning. It is called Dyshidrosis sicca. After recurrent attacks the nails may develop dystrophic changes, irregular transverse ridging and pitting, thickening and discoloration. Keratolysis exfoliative/desquamation en aires is probably a mild pompholyx. During the summer months, small areas of superficial desquamation develop on the sides of fingers, palms and feet.

There is no or little irritation or vesicles.

POMPHOLYX

H. Juvenile plantar dermatosis

Synonyms: Peridigital dermatosis, forefoot eczema, tennis –shoe foot, atopic winter feet

Definition

It is characterized by dry, fissured dermatitis of the plantar surface of the forefoot occurring exclusively in children aged 3 to 15 years.

Etiology

It is unknown. Fungal infection, bacterial colonization, contact allergy and atopy do not have any role. The marked prevalence in summer, the regular history of hyperhidrosis and the frequent use of rubber-sole sized shoe suggest that the process is related to the role of heat, sweating and frictional trauma.

Histopathology

There are features of a mild non-specific eczema, but sweat blockage can be sometimes observed. Moderate acanthosis with hyperkeratosis seen. Important feature is the presence of chronic inflammation around the sweat duct.

JUVENILE PLANTAR DERMATOSES

1. I. Autoeczematization

Synonym: Autosensitization dermatitis

It refers to spread of chronic dermatitis that was previously localized to distant parts of the body. Grouped pruritic papules, papulovesicles and patches of dermatitis are seen on various parts of the body. The onset is usually sudden but maybe gradual. The patient wrongly feels that new dermatitis is an extension of a previously localized chronic dermatitis. Skip areas of normal skin may occur between lesion of primary and secondary dermatitis. It most commonly originates from stasis dermatitis.

Pathogenesis

It is unknown. The finding of increased circulatory activated T-cells and an increased helper/ suppressor T-cell ratio suggested a cell-mediated autoimmune mechanism. A generalized hyperirritable skin is another possibility. Circulatory skin specific cytotoxic antibodies do not have a role.

AUTOECZEMATIZATION

Id (Autoeczematization) Reaction:

Initial Dermatitis was located between the patient’s toes(Picture on left).

Approximately one week later a more generalized pruritic eruption arose on
the patient’s chest (Picture on right)

1. Exogenous eczema
2. A. Contact dermatitis

Definition

It is an inflammatory response of the skin to an exogenous substance (irritant and /or allergen)

Classification

It may be classified as follows:

1. 1. Irritant contact dermatitis
2. 2. Allergic contact dermatitis
3. 3. Contact urticarial
4. 4. Photocontact dermatitis

1. 1. Irritant contact dermatitis

Any physical or chemical agent that is capable of producing cell damage, if applied for sufficient time and in sufficient concentration can lead to irritant dermatitis. This dermatitis process does not involve immunological factors but results when the repair capacity of skin is exhausted or when the penetration of chemicals excites an inflammatory response.

1. Acute irritant contact dermatitis: This condition is produced by strong irritants e.g.; concentrated acids, alkalis or solvents. It usually results following a single exposure but multiple exposures maybe required in some cases. All individuals exposed to strong irritants develop irritant dermatitis. It is a common occupational hazard that often results from poor work habits but maybe due to accidental exposure.

The clinical spectrum may range from mild transient erythema to florid dermatitis with vesiculation. In severe cases, bulla formation and even tissue necrosis may occur as seen in lime or cement burns.

1. Cumulative insult dermatitis

Synonym: Chronic irritant “wear and tear dermatitis”

It is a result of cumulative damage to skin caused by various physical and chemical factors e.g.: friction, low humidity, heat, cold, solvents, soaps and detergents. Susceptibility to develop it depends on extent and degree of exposure, age, site, individual susceptibility. Atopics are more prone to develop this type of dermatitis. It is mainly caused by damage to skin barrier. Once the skin barrier has been broached, even harmless substances can lead to initiation and perpetuation of irritant dermatitis.

It is exemplified by the hand dermatitis caused by detergents in housewives and by cutting oils in machinists. Solvents (e.g.: diesel, kerosene and detergents) used as cleansers often cause chronic irritant dermatitis. Other hazardous occupations are nursing, hair dressing, gardening, house building and dairy farming.

It manifests as localized patches of dry, slightly, inflamed or chapped skin with little tendency to disseminate. It tends to be more static and less pleomorphic than constitutional forms of eczema.

IRRITANT CONTACT DERMATITIS

Irritant contact dermatitis caused by frequent handling of fish

1. 2. Allergic contact dermatitis

History

In 1840, Fuchs understood that external agents were responsible for “dermatitis venenata”, as a result of idiosyncrasy. In 1895, Jadassohn suggested patch testing valuable in establishing the causal factor of dermatitis medicamentosa.Bloch and Steiner Wourlisch used Primula obonica extract to sensitize humans and established the concept of sensitization. Landsteiner and Jacobs (1935) demonstated that haptens become immunogenic, only after conjugation with protein carriers. Lansteiner and Chase demonstrated  that delayed hypersensitivity could be passively transferred with lymphocytes. This concept was further supported by the discovery of B-cells and T-cells. Silberg et al observed that Langerhan cells of epidermis acted as antigen presenting cells for allergic contact dermatitis. This led to a better understanding of the pathophysiology of allergic reaction.

Predisposing factors

1. a. Constitutional factors : Experiments with 2,4-dinitrochlorobenzene(DNCB) indicate that some individuals are resistant to sensitization. This resistance may have been acquired by repeated exposure to subsensitizing doses of the allergen. Certain persons develop sensitivity to nickel; this maybe a genetically determined trait. Siblings and children of patient suffering from contact dermatitis have an increased incidence of positive patch tests implicating constitutional factors as predisposing factors.
2. b. Sex: Women are commonly more hypersensitive to lanolin and nickel due to frequent exposure.
3. c. Age: Less common in children due to lack of exposure
4. d. Hormones: Hormones have been alleged to have some effect as pregnancy and use of oestrogens have been shown to improve or aggravate contact dermatitis.
5. e. Race: Parthenium hypersensitivity is rampant among Indians whereas in United States, the plant is virtually harmless. Negroes are relatively resistant to poison ivy sensitization as compared to Caucasians.
6. f. Environmental factors: Due to cultural and environmental factors, nickel sensitivity is more in women and chromate sensitivity in men. Each age tends to have its own spectrum of sensitivities according to exposure pattern at that time.
7. g. Local factors: if the skin is damaged, sensitivity can easily be acquired as I the cases of burns, ulcers, stasis, eczema etc. the longer the duration of eczema, the greater the incidence of sensitivity. Occlusion promotes percutaneous absorption and probably contributes to the increased incidence of medicament dermatitis in stasis eczema, otitis externa and perianal dermatitis.
8. h. Coincidental disease: Impaired capacity for sensitization may be caused by diseases like lepromatous leprosy, cancer, Hodgkin’s disease, mycosis fungoides, parasitosis and sarcoidosis.

The ecology and epidemiology of contact dermatitis

Contact dermatitis accounts for 4-7% of all cases.  Common sensitizers vary from place to place and time to time. New potential sensitizers increase the incidence of contact dermatitis in a population and at the same time, allergens, which are previously common, disappear due to their non use. Potential sensitizers will give positive reactions in all countries although their ranking may vary e.g.: neomycin is a common sensitizer all over world, but in India nitrofurazone is the commonest and in Singapore, proflavine is the commonest. Cosmetics and fragrant materials are increasingly becoming important sources of sensitivity.

Incidence

Incidence varies from 1.5-6%. In certain trades like construction work, chemical& metal industries, incidence is particularly high. Legal measures can alter the incidence of sensitivity by banning allergens e.g.: PPD in hair dyes is banned in several countries. Seasonal changes can alter incidence as in case of plant dermatitis. In tropical countries, incidence is more in summer and rainy season.

Clinical features

Contact dermatitis can mimic any type of eczematous eruption. It usually develops a few hours after allergen exposure. The skin becomes itchy, swollen and red or dry and bumpy. Blisters may develop, if the reaction is more severe. Blisters may break, leaving crusts and scales. Skin may later flake and crack. Long term exposure causes skin to become thick, red and scaly. Later, the skin becomes dark and leathery. The clinician should ascertain whether it is endogenous or exogenous. A detailed history of occupation, hobbies, personal objects, family history and treatment history and special features of dermatitis produced by different antigens are a prerequisite to arrive at a tentative diagnosis.

ALL    ALLERGEN	PRESE   PRESENT IN
Nickel           Nickel	Jewelle  Jewellery , jean studs, bra clips
Dichro         Dichromate	CemeC  Cement, leather, matches
Rubber        Rubber chemicals	Clothin  Clothing, shoes , tyres
Coloph       Colophony	Stickin    Sticking plaster, collodion
Paraph        Paraphenyldiamine	Hair dy  Hair dye, clothing
Balsam       Balsam of Peru	Perfum   Perfumes, citrus fruits
Neomy       Neomycin, benzocaine	Topical Topical applications
Parabe        Parabens	Preserv  Preservatives in cosmetics and creams
Wood a      Wood alcohols	Lanolin   Lanolin, cosmetics, creams
Epoxy r      Epoxy resin	Resin a  Resin adhesives

Common regional contactants

1. 1. Face:

a)      Cosmetics like face powder, cream , vermilion, bindi, hair dyes etc

b)      Volatile dust, pollens, fumes, paints

c)       Those conveyed by patient’s fingers e.g.: nail varnish

1. 2. Lips: lipstick, toothpaste, cigarette holders, pipes, balloons
2. 3. Neck: scarf, dyed fur, collar, buttons, mark ink, jewellery (chrome  
3. 4. Body: clothing, buttons, marking ink
4. 5. Axillae: dress, armpit pads, dyes, depilatories, deodorants, astringents
5. 6. Genitals and anal regions: contraceptives, toilet paper, douches, nylon/plastic underwear, anti pruritics, feminine hygiene sprays
6. 7. Buttocks: toilet paper, lavatory seat, jute &straw mattresses, toy horses
7. 8. Hands:

a) occupational-primary irritants and sensitisers

b) hobbies- gardening, photography, painting

c) Cutting vegetables- garlic, onion, tomatoes

d) Drivers

e) Detergents

f) Cigarette paper

1. 9. Wrist: watch and its strap, bracelet, bangles
2. 10. Thighs: clothing, pocket objects like matchbox, suspenders
3. 11. Feet: Footwear, shoes, coloured socks, elastic shoe strap

Specific types of allergic contact dermatitis

1. i. Dermatitis from topical medicaments: One third of all cases of contact dermatitis common in patients with stasis eczema, long standing pruritus ani or vulvae, chronic otitis externa and pressure sores. Sensitivity is obvious in nitrofurazone but overlooked in
2. ii. Dermatitis due to metals: Metal dermatitis is most frequently caused by nickel, chromates and mercury. Pure metals except nickel do not cause hypersensitivity.
3. iii. Rubber dermatitis: Usually caused by accelerators, antioxidants and other chemicals used in the manufacture of rubber. Rubber gloves are main source of dermatitis, in addition to condoms, shoes, boots, underwear elastics, belts etc. Keratosis, appear on palms and soles, so called “black rubber hands/ feet”, which disappear rapidly after cessation of use of objects containing sensitizing substance. They have hypersensitivity to black rubber mix (IPPD, CPPD&DPPD). Fisher defined PPPP syndrome as an allergic dermatitis characterized by purpura, petechiae, pruritus and hypersensitivity to IPPD.
4. iv. Plastic dermatitis: Plastic polymerizing agents like curing agents, stabilizers, plasticizers, catalysts, accelerators and antioxidants maybe the irritants. Epoxy resins and phenol formaldehyde plastics cause allergic and irritant dermatitis. Carbamide formaldehyde and acrylic plastics cause allergic reactions and polyester plastics produce irritant dermatitis.
5. v. Clothing dermatitis: Skin problems are attributed to durable press finishes, dyes, rubber additions, chromates, nickel and glues used in cloth manufacturing. The distribution of eruption conforms to a pattern that coincides with places or skin where garments fit most snugly.
6. vi. Plant dermatitis: Catechols and lactones are common plant sensitisers. Poison ivy and poison oak dermatitis are common in North America. Primula sensitivity in Northern Europe and Parthenium dermatitis in India are examples. Dermatitis due to plants maybe occupational or non occupational. Farmers, gardeners, florists and undertakers are common victims. Chrysanthemum, tulips and Narcissae are common causes of occupational exposure. Usually seasonal but with chronicity, it may become perennial with seasonal exacerbations. Usually affects hands, forearms, face, neck, fingertips. A light aggravated dermatitis maybe the presentation. Principal types are irritant, allergic, and phytotoxic; light aggravated and pseudo-phyto-photodermatitis.
7. vii. Wood dermatitis: Carpenters, cabinet makers, joiners, others who saw, sand, turn and plane wood, local timber workers are at high risk. Most of problems are due to lichens on bark, sap, latex, resins, and caterpillars.
8. viii. Dermatitis due to cosmetics: Accounts for 4% of cases. Predominantly affects females. Fragrances and preservatives are the frequent causative agents.
9. ix. Occupational contact dermatitis: Accounts for 20-80% of all dermatoses.

Incidence: In a study of 1551 persons, 11% had occupational contact dermatitis.

Predisposing factors:

1. Job related factors: wet work, irritating chemicals, heat, cold, humidity, vibration, radiation, biologic agents, and trauma.
2. Host related factors: dry, fair skin, ageing skin, hairiness, sweating, atopic eczema, acne, psoriasis, cutaneous allergies, and other skin diseases.
3. Indirect factors: drugs, season of year, personal hygiene, age.

Clinical features:

Manifest as cumulative irritant, allergic or photo dermatitis. Hands are the most common site affected in 80-90%cases. Dust and vapours affect face and neck. Dermatitis of feet and legs, are more often, seen in miners and cement workers.

Diagnosis: Based on treatment history, physical examination and lab investigation.

Prevention: Mainly by pre employment screening and corrective work measures.

1. x. Systemic contact dermatitis: Due to systemic administration of contact allergens or immunochemically related substances, a generalized eczematous eruption is produced in a sensitized individual. This is called systemic contact dermatitis.

1. xi. Non eczematous contact dermatitis: Usually allergic dermatitis present as eczematous but occasionally it is non eczematous, viz. urticarial, granulomatous, acneiform, hyperkeratotic, pigmented, and purpuric. Various manifestations are erythema multiforme-like eruptions, purpuric contact dermatitis, pigmented contact dermatitis, lichenoid contact dermatitis, acneiform eruptions, contact halogenosis, contact granulomas and miscellaneous.

ALLERGIC CONTACT DERMATITIS

Allergic contact dermatitis due to metal belt buckle and nickel in jewellery

Work boot dermatitis Contact dermatitis from poison ivy

Allergic contact stomatitis on the gingiva in a patient with a positive patch test result to nickel, palladium,and mercury.

1. 3. Contact urticaria

It refers to a weal and flare response elicited usually in less than 30 minutes when certain substances come in contact with the skin. Great variety of materials from macromolecules to simple chemicals can induce contact urticaria. Some affect normal skin while some affect damaged skin.

Types

Based on mechanism of causation, there are 3 major types:

a)      Non-immunologic contact urticaria: It is most common, least serious and occurs in all exposed individuals. A direct influence on dermal vessel walls or non immunologic release of vasoactive substances such as histamine, and bradykinin maybe the probable cause. Certain preservatives, flavouring agents are primarily urticariogenic agents. Strongest urticariogenic agents are benzoic acid, sorbic acid, cinnamic acid and cinnamic aldehyde. Caterpillar hair, moths, plant nettles, arthropod stings and bites may produce contact urticaria. The most common test is the open test in which a small amount of test substance is applied to the volar aspect of intact skin of forearms. The result is recorded after 30-45 minutes.

b)      Immunologic contact urticaria: The criteria are past uneventful history of exposure, low proportion of exposed individuals, is affected and positive passive transfer. It is more common among atopics and in damaged skin. Most common immunologic mechanism is probably the one mediated by IgE, specific IgG and also IgM. It is produced by agents like foods, topical medications, metals, rubber, chemicals, animal appendages and secretions, industrial chemicals, textiles.

CONTACT URTICARIA

Contact urticaria of lip due to food allergy, tongue in a patient with latex allergy, from latex gloves

1. 4. Photocontact dermatitis

This form of eczema is immunologically based. It is elicited in persons who have been sensitized by previous exposure to photosensitisers and at the same time to light. There are many potential photosensitizing drugs like phenothiazines, topical non-steroid anti-inflammatory drugs and topical sulphonamides.

PHOTOCONTACT DERMATITIS

Sun exposure after drinking lime juice cause Photocontact dermatitis

Severe lime dermatitis in a bartender mixing drinks and working in the sunlight

B. Infective dermatitis

Synonym: Infective eczema, infectious eczematoid dermatitis

Definition

It is an eczema caused by contact with microorganisms or their products.

In this condition, a bacterial, viral or fungal infection is the primary event, followed by secondary eczematization.

Pathogenesis

Bacterial agents can promote or cause a cytotoxic reaction in skin. They also aggravate or perpetuate rather than initiate the dermatitis. Cultural staphylococci applied topically, can provoke an eczematous delayed hypersensitivity reaction.

Pathology

The histologic picture is that of a subacute or chronic dermatitis. In some cases, subcorneal pustulation is conspicuous. The dermal infiltrate may contain numerous neutrophils as well as lymphocytes and monocytes.

Clinical features

It occurs around discharging wounds and sinuses, ulcers or intertriginous area. Poor hygiene, sweating, maceration, friction with clothing and scratching, all favours its development. It manifests as an area of erythema with tiny vesicles. Later on, oozing and crusting with an underlying raw area can be seen. Fissuring occurs easily if there is involvement of the skin folds.

Typical clinical presentations

1. Retroauricular dermatitis, presenting as chronic fissuring and crusting behind ears. Occurs in young girls. Occlusion of the area by hair or friction with spectacle frame may play a part in localization. Redness, crusting and scaling may involve adjacent scalp.
2. Infective dermatitis of the feet mainly affects the medial interdigital spaces and dorsum of medial toes. Streptococci and staphylococci are usually cultured from these spaces.
3. Infective dermatitis of lower leg is common in patients with venous leg ulcers.
4. Infective dermatitis around a discharging sinus or wound and extends far from it.
5. Infective dermatitis may be complicated by chronic threadworm infestation, pediculosis or scabies.

Diagnosis

The main diagnostic problem is differentiated from contact dermatitis, especially reactions to topical medicaments or from clothing or shoes. A detailed history must be obtained and patch tests are essential. The examination of scraping from the margin/may occasionally is necessary to exclude fungal infection. The isolation of bacteria merely provides confirmation of colonization. The possibility that the infective dermatitis has complicated preexisting dermatoses must be always considered.

INFECTIVE DERMATITIS

C. Radiational eczema

Definition

Dermatitis produced by excessive doses of X-rays received by the skin.

It was common in past with crude X-ray machines and inexperienced people. Acute radio-dermatitis is rare and depends upon the degree of burn and varies from erythema, scaling, vesicular or bullous reaction to ulceration. In chronic cases, there is a long latent period of months and years, followed by redness, telengiectasia, pigmentation and atrophy. In severe cases, ulceration and epitheliomas may develop.

D. Photodermatitis

Dermatitis is confined to exposed parts of body like face, neck, ‘V’ of chest, hands, external surfaces of forearm, dorsum of feet and the adjoining parts of legs. The integument is sensitive to sunlight and UV rays. Seasonal variations are important in countries with extremes of climate.

Etiology

1. Drugs like sulphonamides, chlorpromazine, promethazine, terramycin, declamycin, chlorthiazide, diuretic, hypotensive and antidiabetic drugs, quindexin in animal feeding stuff.
2. Foods like figs, buckwheat
3. External application of bithional, tetrachlorsalicyclanilide
4. Plants and their products like parsnips, meadow grass, mustards, lime oil, celery etc
5. Vitamin B complex deficiency
6. Porphyrinuria
7. Seborrhoeic diathesis
8. Liver disorders

Pathology

Acanthosis and spongiosis are seen in the epidermis. Characteristically, there is an upper dermal dense, lymphatic perivascular infiltrate with hyperchromatic convoluted nuclei and mitotic figures. The picture, closely simulate, a T-cell lymphoma.

Clinical features

It commonly occurs in elderly men, occurring either in normal subjects or with preexisting skin condition. There is often a sharp border at the edge of clothing. Sparing of upper eyelids, fingers, webs, retroauricular and submental regions and skin creases is striking. Itchy, discrete or confluent, eczematous plaques with lichenification are resent. These maybe associated with erythematous, shiny infiltrated papules. The lesions usually persist but may occasionally evolve into erythroderma.

Diagnosis

The diagnosis of a photosensitive eruption in a patient is based on history and clinical examination and can further be corroborated by histopathological examination of the lesions, phototests and photopatch tests. Some patients require routine and special biochemical tests as well.

PHOTODERMATITIS

1. E. Phytophotodermatitis /Berloque dermatitis

Photosensitization of skin, after contact with plants, which are either photo-toxic or photo-allergic action, results in phytophotodermatitis. Clinically, the lesions consist of a linear erythematous, bullous rash which heals in a week or two. On healing, pigmentation is left behind, which takes several months to disappear. The rash develops after contact with plant followed by exposure to sunlight.

Diagnosis

It is done by patch testing of leaves (1cm² piece of leaf) or active ingredients or standard concentration of extracts of plants. The allergenicity of a plant varies according to season and between two plants of the same species.

PHYTOPHOTODERMATITIS

Phytophotodermatitis caused by exposure to wild parsnip and sunlight and Ficus carica.

1. F. Eczematous dermatophytosis

This is due to an allergic reaction to a dermatophyte infection elsewhere in the skin. A classical example is where a person has localized fungal infection of the feet, which is later followed by a widespread generalized eczematous eruption. The most common dermatophyte infection is tinea pedis (athlete’s foot). The primary lesion is a vesicle or papule and there maybe maceration of web spaces. Tinea of the hand (tinea mannum) is characterized by red papules and thick scaling of the palms. Tinea mannum can occur when there is an explosive flare of the feet tinea. Vesicular tinea has very few vesicles.

Diagnosis: Patient has a negative KOH preparation.

ECZEMATOUS DERMATOPHYTOSIS

Dermatitis, reaction to tinea

G. Dermatophytide

A Dermatophytide is an allergic reaction, caused by an inflammatory fungal infection at a distant site. The rash is usually itchy like dermatitis, with bumps or blister scattered on face, trunk and/or limbs. Fungus cannot be cultured from an ide.

Clinical features

1. Scattered small spots centered on hair follicles mainly affect the trunk, usually follows a kerion (inflammatory tinea corporis or tinea capitis) or from a zoophilic (animal fungus).
2. Crops of fluid-filled blisters on the palms and back of the hand resembling pompholyx may arise as a result of severe tinea pedis or other dermatophyte infection
3. Erythema nodosum may follow severe tinea

DERMATOPHYTIDE

Case1: Widespread rash        Primary zoophilic dermatophyte infection          Crusted itchy papules

Case 2: Athlete’s foot                    Clusters of papules on knees         Clusters of papules on knees

H. Secondary eczematization

It is the occurrence of eczema secondary to a preexisting dermatosis.eg: following scabies, pediculosis, insect bite, allergy etc

Hand and Foot eczema

The hands and feet are the frequent sites of inflammatory eruption. The hands because they are frequently, subjected to mechanical and chemical trauma; the feet due to the warm, moist conditions in shoes.

Definition

Hand and foot eczema denotes a variety of disease entities showing inflammation of the hands or feet caused by exogenous or endogenous agents.

Classification

a) Etiological classification

b) Morphological classification

1. Pompholyx
2. Recurrent focal palmar eczema
3. Hyperkeratotic palmar eczema
4. Ring eczema
5. Wear and tear dermatitis(dry palmar eczema)
6. Fingertip eczema
7. Apron eczema
8. Discoid eczema
9. Gut eczema
10. Juvenile plantar dermatosis

Epidemiology

The true incidence is not known but females showed a higher rate of positivity than males. Vegetables were the most common sensitizers, followed by soaps and medicaments. Among the vegetables, garlic and onion were the most potent sensitisers. In majority of the patients, occupational allergens were the cause of hand dermatitis.

Etiology and pathogenesis

Its origin ranges from bare-handed work with guts in a slaughterhouse to wearing gloves in the operating room. Detecting the cause requires good history taking and patient orientation. It is more common in patients with an atopic background. Altered sensitivity of atopic patients to exogenous allergen contactants and impaired barrier function of their skin are probable contributory factors.

One type of irritant dermatitis is caused by a single application of a strong chemical substance resulting in acute toxic reaction (chemical burn). A second type is caused by repeated applications of one (or more) irritants, which will not elicit any visible skin reaction in a single exposure. Chapping, erythema craquele and haemorrhagic fissures of the skin are the manifestations. Clinical signs are reversible as soon as the irritant influence ceases. Most cases of irritant dermatitis in occupational dermatology are of this type. A third type of irritant dermatitis is caused by the same repeated low grade irritants, but because of unknown constitutional factors, chronic spongiotic dermatitis develops. Thus the dermatitis is caused and maintained by irritant.

Hand and foot eczema is exacerbated by further exposure to irritants. Eczema of the dorsum of hand is more often irritant or atopic than allergic. A combination of HLA-A3 and HLA-B7 appears to make an individual more sensitive. Bacterial infections complicate eczema. Stress is a major contributory factor in the development of a recurrence especially pompholyx but pathogenesis unclear.

Clinical features

The salient features of primary dermatoses involving the hands and feet are:

1. Pompholyx : Pinhead sized, non inflammatory vesicles situated on the tips or sides of the fingers are seen at the onset. Vesicles are also seen at the edge of the eczematous plaque. Large multiloculated bullae can develop by coalescence of multiple vesicles. Through the process of Autoeczematization, it spreads to palms and dorsal surface of fingers. If left untreated, the entire hand becomes involved. Dyshydrotic eczema of the foot is distinguished by its onset as minute, non inflammatory vesicles. Dyshydrotic eczema of the feet is a particularly common problem in children.
2. Atopic dermatitis: The initial lesions are found on the dorsal surface of the hands or feet. Later, Autoeczematization, lead to varying degree of palmar or plantar involvement. The plaque of atopic dermatitis, are often sharply marginated and nummular.
3. Allergic contact dermatitis: It always begins on dorsal surface. The predilection is probably due to the protective effect of the thick keratin found on the palms or soles. It differs from atopic dermatitis in that excoriations are less prominent and a visible eruption precedes the scratching.
4. Irritant contact dermatitis: It is characterized by presence of chapping, cracking and fissuring, mostly noted on palms and knuckles. The skin is dull red in colour and has a shining or glistening appearance. Tingling or burning pain is present; pruritus is minimal. The diagnosis is based on the clinical the clinical appearance and on the history of frequent exposure to soap water or other solvents. It is an occupational hazard for mothers, housewives, nurses, dentists, waitresses, bartenders, industrial workers. Irritant dermatitis of the feet usually because of maceration secondary to sweat retention. This condition is particularly likely to occur in individuals with hyperhidrosis of the feet and in those who wear shoes which retard evaporation from the skin. So, it is an extraordinarily common in problem in children who wear tennis shoes all day long.
5. Keratolysis exfoliativa: It is a common chronic asymptomatic non inflammatory bilateral peeling of the palms and soles. Exact cause unknown. The eruption is commonly associated with sweaty palms and soles. Some people experience this ailment only once, whereas others do so recurrently. Scaling starts simultaneously from several points of the palms and soles. The scales continue to peel and extend peripherally, forming larger roughly circular areas that resemble ringworm, while the central area become slightly red and tender. The condition resolves spontaneously within a span of few weeks and deserves no therapy except lubrication.
6. Hyperkeratotic eczema: It is a very thick, chronic form of eczema that occurs on the palms, occasionally on the soles, seen almost exclusively in men. One or more several plaques of dense yellow brown scales increase in thickness and develop deep interconnecting cracks on the surface. This type of eczema may result from allergy or excoriation and irritation, but exact cause unknown. The disease is chronic and to be treated like chronic eczema.
7. Fingertip eczema: It is a very dry chronic form of eczema of the palmar surface of the fingertips. It may result from an allergic reaction to plant bulbs or resins, but may also occur as an isolated phenomenon of unknown cause. One or more several fingers maybe involved. Initially the skin maybe moist, but later it becomes dry, cracked and scaly. The skin peels off from the tips distally, exposing a very dry, red, cracked, fissured, tender or painful surface without skin markings. The process extends upto the distal interphalangeal joint. Fingertip eczema is often recalcitrant. It should be managed as subacute or chronic eczema.
8. Ring eczema: It occurs predominantly in young ladies and rarely men. It usually starts soon after marriage or childbirth. An irritable patch of eczema develops under a ring, usually a broad wedding ring, and tends to spread in a typical manner to involve the adjacent sides of the middle finger and the adjacent area of the palm. This type of eczema is probably due to concentration of soap and detergent beneath a ring, but microtrauma especially friction maybe a precipitating factor.
9. Housewives’ eczema (wear and tear dermatitis): According to Fisher, it is probably the most common type of contact dermatitis of the hands in clinical practice. It occurs principally on the fingers, the interdigital spaces, palms and the back of hands. It occurs in housewives doing cleaning and cleansers, hotel-kitchen workers, dish washers, dentists and surgeons. Feet are also involved, when housewives do household work in the squatting position, in India.

The first change is dryness, followed by redness and scaling first on the palms, but later on the dorsa of the fingers, particularly on the knuckles and interphalangeal joints. Later on superficial cracks develop on a background of erythema. Oozing, crusting and frank eczematization follow. Secondary infection may complicate. The condition maybe associated with fingertip eczema or ring dermatitis. In chronic cases, lichenification develops eventually. Atopics are prone to develop hand eczema because of their xerotic skin.

1. Apron eczema: It is a type of hand eczema which affects the proximal palmar aspect of two or more adjacent fingers and the adjacent palmar skin over the metacarpophalangeal joints, resembling an apron. This pattern of eczema is mostly due to an endogenous eczema.
   1. Gut or slaughterhouse eczema: It involves workers who eviscerate and clean pigs’ carcasses in a slaughterhouse. It begins in the finger webs and spreads to the sides of the fingers. This self limited condition spontaneously resolves within a week or two, even if the patient continues his work, but can recur in future.
   2. Acrodermatitis enteropathica:

Synonyms: Brandt syndrome/Danbolt-Cross syndrome/Congenital zinc deficiency

It is an autosomal recessive metabolic disorder affecting the uptake of zinc, characterized by periorificial (around the natural orifices) and acral (in the limbs) dermatitis, alopecia (loss of hair), and diarrhea. Similar features may be present in acquired zinc deficiency. This disease also is related to deficiency of zinc due to congenital causes.

Features of acrodermatitis enteropathica start appearing in the first few months of life, as the infant discontinues breast milk. There are erythematous patches and plaques of dry, scaly skin. The lesions may appear eczematous, or may evolve further into crusted vesicles , bullas or pustules. The lesions are frequent around the mouth and anus, and also in hands, feet and scalp. There may be suppurative inflammation of the nail fold surrounding the nail plate – known as paronychia. Alopecia may occur. The skin lesions may be secondarily infected by bacteria such as Staphylococcus aureus or fungi like Candida albicans. These skin lesions are accompanied by diarrhea.

1. Acrodermatitis chronica atrophicans (ACA):

Synonyms: Herxheimer disease, Primary diffuse atrophy

It is a skin rash indicative of the third or late stage of European Lyme borreliosis.ACA is a dermatological condition that takes a chronically progressive course and finally leads to a widespread atrophy of the skin. Involvement of the peripheral nervous system is often observed, specifically polyneuropathy.

This progressive skin process is due to the effect of continuing active infection with the spirochete Borrelia afzelii. B afzelii is the predominant pathophysiology, but may not be the exclusive, etiologic agent of ACA. Borrelia garinii, has also been detected. The rash caused by ACA is most evident on the extremities or limbs beginning with an inflammatory stage with bluish red discoloration and cutaneous swelling and concluding several months or years later with an atrophic phase. Sclerotic skin plaques may also develop.

As ACA progresses the skin begins to wrinkle.

Diagnosis

It can be investigated by alkali resistance test, Locher’s Nitrazine yellow test, Patch test, Hand immersion test.

HAND AND FOOT ECZEMA

Fingertip eczema                      Keratolysis exfoliativa     

The secondary dissemination of eczema

A very characteristic feature of eczema is its tendency to spread widely from its point of origin. It spreads either by (i) external contact (ii) ingestion or injection of an allergen, (iii) haematogenous dissemination from a primary focus.

1. In many cases, extension is merely the result of continued contacts of new area of skin with a specific external allergen. With increasing degrees of allergic sensitivity, minimal contact may provoke an eczematous response. The pattern of extension in such cases is asymmetrical and its progress is irregular. E.g. contact dermatitis of lower leg induced by lanolin sensitivity, spread to the hand applying the ointment and as a result of casual patches may appear on face.

1. In other cases, an eruption originally induced by sensitivity to a topical medicament may relapse after ingestion or injection of the same drug. This eruption tends to be widespread, more or less symmetrical and of sudden onset. Previously affected sites maybe preferentially affected and traumatized sites may also be involved. The diagnosis maybe suspected in a widespread recurrent eczema which does not conform to recognized patterns of endogenous eczema and yet cannot be related to external contact or to dissemination from a primary focus. Such eruptions may be induced by penicillin and by other drugs. Recently traces of chromate in certain foods have also been incriminated.

1. A more common phenomenon is the sudden haematogenous dissemination of a localized eczema. It occurs most frequently from lower leg, foot and thigh. The eczema may have been present for a few days or many years. Dissemination is often immediately preceded by an exacerbation with increased inflammatory changes at the primary site, usually occurs explosively. Morphologically, the secondary eruption may at first consist of small, oedematous papules. They soon become eczematous and grouped papulovesicles may become confluent in small plaques. Occasionally, lesions form erythematous macules or weal. Distribution is symmetrical and its pattern is influenced by the primary site, duration and severity of the reaction.

The course of the secondary eruption depends upon largely on the progress of the primary lesion, but maybe influenced by systematic factors. If the primary lesion is maintained in an acute inflammatory state, the eruption increases in severity and may become generalized. If the patient is rested and the local lesion allowed to settle, the secondary eruption will subside, but will often recur readily, if the local lesion is allowed to relapse. In few patients with reticulosis or leukaemia, the generalized secondary eruption evolves into erythroderma, which maybe self-perpetuating. The mechanism of secondary dissemination is by contact sensitivity, bacterial sensitivity, auto allergy or through influence of primary site.

Investigations

The three important steps in dermatological diagnosis are:

1. Morphological diagnosis – based on morphological study, localization and distribution
2. Clinical diagnosis– establishment of disease based on history and clinical features.
3. Etiological diagnosis –establishment of cause or causes in the patient.

Generally, investigations of eczema include:

1. A. Clinical diagnosis: By clinical features and detailed case taking including history of present illness, past illnesses, personal history, family history and treatment history.
2. B. Routine blood tests and immunological tests: It is done to support the diagnosis of atopic eczema and to determine specific environmental allergens. E.g.: house dust mite, pollen, foods etc.
3. C. Patch tests : It detects type IV(delayed or cell mediated) hypersensitivity. Introduced by Jadassohn and it is the only scientific method to detect the cause of contact dermatitis. A ‘battery’ of around 20 common allergens is applied to the skin of upper back under aluminium disc for 48 hours. The sites are then examined for a positive reaction 24 hours later and possibly, again a further 24 hours later. An eczematous reaction, in the absence of an irritant reaction, suggests, a type IV hypersensitivity, to that particular allergen.

Evaluation of patch test readings

+ or ?	Doubtful reaction	Faint erythema only
+	Weak (non vesicular)positive reaction	Erythema, infiltration andpossibly discrete papules
++	Strong (vesicular) positivereaction	Erythema, infiltration,papules and vesicles
+++	Extreme (bullous) positivereaction	Intense erythema,infiltration and coalescing  vesicles
Negative	+IR Irritant reactions	NT Not tested

The relevant antigens for a particular clinical case may not be represented in the standard battery of tests and expert advice maybe needed. A negative patch test does not exclude a pathogenic role for a particular antigen nor does the response to an antigen mean that this antigen is causing the clinical disease.

1. D. Prick tests

They are a way of detecting cutaneous type I (immediate) hypersensitivity to various antigens such as pollen, house dust mite or dander. The skin is pricked with commercially available stylets through a dilution of the appropriate antigen solution. After 10 minutes, a positive response is indicated by a weal and a flare. A positive control (histamine) and a negative control (antigen diluents) should be performed. Systemic antihistamines inhibit the magnitude of the reaction. In individuals, with a clear history of particular type I hypersensitivity, a systemic reaction may follow a prick test and resuscitation facilities should be available. As an alternative test, specific IgE levels to antigens can be measured in serum by a specific radioallergoabsorbent test (RAST).

1. E. Bacterial and viral swabs for microscopy and culture

These are useful tests in suspected secondary infection. Skin swabs for bacteriological assessment will invariably reveal the presence of bacteria, but antibacterial treatment is reserved for those cases with evidence of clinical infection. In the case of recurrent impetigo in a child with atopic eczema, bacterial swabs should be taken from the carrier sites (nares, axillae and groin) from both the affected individuals and all household members.

1. F. Phototesting

It involves exposing skin to a graded series of ultraviolet radiation of unknown wavelength, either on one occasion or repeatedly. In many photodermatoses, erythema will occur at a lower dose than in normal population or the time course of erythema maybe prolonged. It is an essential investigation of patients with presumed photosensitive drug reactions and idiopathic photodermatoses.

Other tests include histological examination, diascopy, epiluminescence microscopy, Wood’s light, immunofluorescence, electron microscopy, mycology sampling.

Differential diagnosis

1. Allergies
2. Food allergies
3. Vitiligo
4. Diabetic dermopathy (stasis dermatitis)
5. Vesicula tinea (dyshidrotic eczema)
6. Scabies(dyshydrotic eczema)
7. Nonsteroidal anti inflammatory drugs(dyshidrotic eczema)
8. Skin rash of undiagnosed diabetes
9. Tinea pedis(dyshydrotic eczema)

10.  Impetigo

11.  Psoriasis

12.  Candidiasis

13.  Drug eruption

14.  Pityriasis rosea

15.  Viral exanthems

16.  Mycosis fungoides

17.  Actinic reticuloid

18.  Grover’s disease

19.  Erythroderma

20.  Blaschko dermatitis

21.  Toxic shock syndrome

22.  Sulzeberger-Garbe syndrome

23.  Polymorphous light eruption

24.  Pigmented purpuric dermatoses

25.  Popular Acrodermatitis of childhood

26.  Erythema annulare centrifugum

27.  Insect bite

28.  Spider bite

29.  Bullous pemphigoid

30.  Cicatrial pemphigoid

31.  Eosinophilic folliculitis

32.  Idiopathic eosinophilic spongiosis

33.  Pemphigus

34.  Malarial spongiosis

35.  Follicular spongiosis

36.  Cellulitis (stasis dermatitis)

37.  Id reaction (dyshydrotic dermatitis)

Management

General management

The general measures of management include:

1. Correct diagnosis, establishment of the cause and sincere attempts to eliminate or correct causes
2. Reassurance to the patient and relatives so as to allay their anxiety about infectivity, severity, scarring and chances of recovery.
3. Specific and palliative treatment

i)        General measures: In simple cases, psychotherapy is done. In complicated cases, and psychotic patients, the help of a psychiatrist is valuable. Spices, hot condiments, non vegetarian foods, tea, coffee and alcohol predispose to sense of heat and to several dermatoses. Simple nourishing and wholesome food is recommended. Restrictions may be necessary in allergic and seborrhoeic condition. Environment should be maintained at a constant temperature. It should be clean and hygienic. Clothing should be adsorbent and non irritating (cotton). Adequate rest and relaxation are important.

ii)      Internal: Systemic drugs like calcium gluconate, corticosteroids and ACTH, sedatives, hypnotics, antibiotics, vasodilators.

iii)    Local: Topical measures like emollients and moisturizers, topical steroids.

iv)    Physical treatment and surgery(if required), protective bandages(only in exogenous eczemas)

1. A. Acute eczema

Treatment must aim first at removing or reversing the cause. The essential principals of management are rest, protection, bland applications, explanation, reassurance and sedation.

a)      Rest should be complete or local according to the severity and extent of eczema. An affected leg should be elevated or well supported and hands should be used as little as possible. In extremely acute eczema, sling is useful and complete bed rest is advisable for severe eczema of the feet or widespread eczema of the limbs or trunk.

b)      Advise patient to avoid all precipitating factors and irritants

c)      Advise patient to avoid frequent bathing/washing especially frequent hot water bath.

d)     Advise patient to avoid oppressive clothing and vigorous rubbing.

e)      Advise patient to avoid ointments and emollients, which act as an obstruction

f)       Use of bland soaps/moisturizers especially after a bath is encouraged.

g)      Eczema should be managed with wet dressings or compresses like normal saline or potassium permanganate solution (1 in 8000 dilution of potassium permanganate/1% solution of boric acid). Gentle cleansing of skin is advisable.

h)      Acute and disseminated eczemas heal quicker on restricted salt and light diet, to eliminate toxic products like milk and rice for 3 days. Endogenous eczemas and urticarias, bland vegetarian diet with restricted coffee, tea, and alcohol is helpful, if continued for 4-12 weeks.

1. B. Subacute eczema

If an acute eczema has failed to clear almost completely in 3-4 weeks, the perpetuating factors should be clearly sought. Continual severe irritation, scratching and rubbing especially in endogenous eczema suggest recurring emotional stress. So counseling should be done. Admission to hospital is advisable, if treatment is not effective. Applications of creams, ointments and pastes are advisable. All dressings should be firmly applied but light and comfortable. In some cases of Asteatotic and nummular eczema, baths may be poorly tolerated and should be restricted. Treatment should not be stopped until healing is complete and patient should be warned that his skin will be extremely vulnerable for some weeks. Warmth or stress may induce pruritus and rubbing may cause further break down.

1. C. Chronic eczema

Persistent eczema is a cause of severe anxiety and a fall in living standards, through loss of employment. So these factors must be carefully assessed. The possibility of underlying skin disease should be excluded. Admission to hospital is helpful for a detailed assessment. Emollients and moisturizers may soothen. Occlusive dressings are useful. The skilful psychological handling of the patient is a vital factor in successful management.

Treatment of specific eczemas

a) Atopic dermatitis

General instructions for atopic eczema patients:

1. The patient should avoid and control precipitating and aggravating factors like sudden change in temperature, reduced humidity, excessive sweating, contact with irritating substances(e.g.: wool) and emotional instability.
2. The patient should have a warm starch bath in winter and a cold Condy’s bath in summer. After the bath, he should blot himself with a smooth towel and avoid rubbing. Olive oil or lanoline cream may be applied on the dry, thickened skin after the bath.

In generalized dermatitis or dryness of skin, oil, butter or ghee massage for about an hour before a bath, help lubricate and soften ski. Emollients should be applied immediately after bath to trap the water in skin. Frequent application of bland lubricant smoothens and protects skin. It is the most important single measure in the therapy of atopic dermatitis.

1. Moderate temperature suits the patient best, so extremes should be avoided.
2. The patient should not scratch and keep his nails short. In resistant cases like in children, measures for physical restraint by splints should be employed and sedatives given at night.
3. The diet should be light. The exact composition of the diet depends upon the history of the patient, the diet diary and the results of the allergy test. Allergenic food stuffs should be avoided. The single factor eliminative diet and a diet diary are two useful measures. In the former, we start the patient on one foodstuff, like boiled milk. If the disease persists, he is given boiled rice and sugar. After the disease has been controlled on boiled milk or rice, every 3 days, one more foodstuff is added, starting with essential ones like wheat (chapattis and bread), fats (butter and ghee), muttons, eggs, peas, carrots, bananas, potatoes, lentils till either an allergic attack develops meaning that the patient is sensitive to the last added food stuff or the normal diet is reached. Usually patients are sensitive to protein diets or vegetables and fruits, preservatives, adulterated food stuffs. Starch, fats and minerals makes poor food allergens.

Diet diary means a specimen chart is maintained for a month or two depending upon the case. Every foodstuff taken during the day is marked by a cross, and at the bottom of the column, the patient puts down whether he felt better or worse, or suffered from an acute flare up; the cause can be discovered. The diet diary is a simple and non cumbersome procedure through which the cause of diet allergies can be found out.

1. The patient should not fatigue himself physically or mentally.
2. Healthy hobbies and play should be encouraged. They help to divert attention and speed up recovery. Children should not be allowed to play with fluffy toys, grass, flowers and chemicals.
3. Side effects of any medicine should not be reported to physician.
4. Short term hospitalization is often efficacious and the condition may show improvement even before therapy is started.
5. Patient should learn to live within limits of his mental and physical strength, knowing his inborn weakness.

Symptomatic treatment: By antihistamine, systemic steroids, evening primrose oil, antibiotics and photochemotherapy.

Treatment for infantile eczema

1. The diet must be corrected, breast –feeding stopped and powdered milk substituted. Other foodstuffs should not be added quickly.
2. Physical restraint to prevent scratching, with the help of splints and bandages
3. Palliative treatment. Use of steroids should be restricted.
4. General state of nutrition must be maintained and sedatives are standby.
5. The child should be bathed in 1 in 8000 warm Condy’s solution or bran bath, and then, blotted dry with a smooth towel. If water is not tolerated, the tender skin may be cleansed with a little boiled milk. Following this, a simple talcum powder or prescribed cream or lotion may be used. Strong ointments are harmful.
6. Cardboard splints maybe necessary to prevent the child from scratching and damaging the skin. Hands should be restrained by bandages or mittens at night.
7. Normal diet maybe given excluding allergic foodstuffs. Diet diary or single foodstuff eliminative diet is useful.
8. Healthy play should be encouraged to divert child’s attention. Child should not be allowed to play with fluffy toys, grass, flowers and weeds.
9. Fresh air and mild sun are usually beneficial
10. Woolen garments should not be worn next to irritated skin.

b) Seborrhoeic dermatitis

The goal of treatment is to loosen and remove scale and crust, prevent skin infections, as well as reduce the inflammation and itch. Treatment varies by age and the area of the body to be treated:

1. Infants (scalp): Cradle cap can usually be controlled by shampooing more frequently with a baby shampoo and by softly brushing away the scales. A mild corticosteroid or antifungal medication is advised.
2. Infants(beyond scalp): A mild corticosteroid or antifungal cream is prescribed if condition spreads beyond scalp
3. Adolescents and adults (scalp): African-American patients often get relief by shampooing once in a week. Caucasian patients find shampooing more frequently than usual and leaving the lather on the scalp for a longer time clears the condition. Shampoos specially formulated for dandruff relief are often effective. Sometimes, alternating different shampoos give relief.
4. Adolescents and adults (beyond the scalp): Atopical corticosteroid antifungal medication and phototherapy maybe advised.

Patients are advised to consume more milk, eggs, fish, mutton, chicken and also to add green vegetables and fresh fruits. They should cut down and fat rich fried food stuffs like purees, white bread, porridge, rice, potatoes, bananas, mangoes, cake, puddings, pastry, nuts and cheese. Condiments, sauce and pickles should also be avoided.

c) Asteatotic eczema

Bathing should be limited. A moisturizer should be applied just after a bath. For erythema or dermatitis, a mid to high potency steroid cream is applied for several days.

d) Nummular eczema

Lesions on lower extremities, takes more time to heal completely. The skin should be protected from further injury. Hydrate the skin by taking a short lukewarm bath or shower once a day and immediately applying a cream or ointment to still damp skin. It can help hydrate as well as relieve the itch and scaling. Medications like topical corticosteroids, tar preparations, antibiotics, antihistamines, and phototherapy may help.

To prevent recurrence, once the skin clears, following measures are recommended:

1. Moisturizing: apply a moisturizer at least daily and after bathing helps, especially in hot climate.
2. Avoid certain activities, which dry heats or irritate skin like hot baths, frequent bathing or sitting next to fire, can cause a flare up.
3. Use a mild non drying cleanser instead of soap, when bathing helps.
4. When heating or air conditioning is necessary, use a humidifier to add moisture to air.
5. Wear loose clothing; avoid wearing rough fabrics such as wool which can irritate the skin.

e) Pityriasis alba

Patients having a tendency to develop this disorder should keep their skin well hydrated. Daily use of an emollient tends to minimize the occurrence. Minimizing bathing time is also beneficial. A weak steroid hastens resolution in the early phase, when there is active inflammation.

f) Stasis dermatitis

Venous pressure should be reduced by avoiding standing still, elevation of feet while sitting and sleeping and wrapping a crepe bandage or stocking on the feet and lower legs, if standing is necessary. Avoid scratching and strict bed rest, if necessary. ‘Pinch’ or ‘postage stamp’ split thickness grafting may be performed for recalcitrant ulcers. Macromolecular dextran beads are also used for non healing ulcers. Petroleum jelly, low dose topical steroid and antibiotics are also recommended.

g) Lichen simplex chronicus

The cause of psychic stress should be inquired into and the patient should be explained the cause of itch-scratch cycle. Atopical steroid with or without antibiotics and antidepressants are helpful. Applying ice to the area instead of scratching helps. Tight fitting fabrics and wool, becoming overheated and stress should be avoided. Fingernails should be cut short.

h) Pompholyx

Cold wet compresses, topical steroids, antibiotics and antihistamines are used. Draining large blisters relieve pain. PUVA therapy recommended in chronic dyshydrotic dermatitis. Lifestyle changes including reducing stress, avoiding allergens, irritants, excessive sweating and dry conditions protect the skin from further injury.

i) Juvenile plantar dermatoses

Change of foot wears (non porous) to use of 100% cotton socks and leather shoes and sandals will help. In severe cases with cracking and severe exacerbation, bed rest may help.

j) Autoeczematization

It depends upon the partial or complete clearance of the original site of chronic dermatitis. In addition, concomitant treatment of distant site with a topical steroid is helpful.

k) Contact dermatitis

The first step is identifying the possible allergen or irritant and then avoiding it by reduction of skin contact or ingestion of it, in case of food allergy, avoiding exposure to sun or artificial light or taking photosensitizing drugs in case of photodermatitis. Lifestyle changes, regular use of emollients, protective clothing, and strict bath measures are effective. In occupational dermatoses, identify materials and chemicals of potential skin toxicity, preplacement examination of workers, worker education and use of protective gear helps. Following a skin care program prevents recurrence.

l) Photodermatitis

Photoprotection is useful. Gradually increasing doses of UVB or PUVA may be employed to desensitize the skin. Topical steroids, beta carotene, antimalarial drugs and oral psoralens are useful.

m) Dermatophytide

Topical steroids and emollients are helpful. Primary fungal infection requires an oral antifungal medication or topical antifungal agent.

n) Infective dermatitis

Treatment is directed at the primary infection that led to dermatitis. Any underlying local or systemic disease should be treated and predisposing factors eliminated. In acute exudative lesions or flexural involvement, saline or potassium permanganate soaks are helpful. Antibiotics and topical antibacterials may be required.

• o) Hand and foot eczema

Waterproof heavy-duty vinyl gloves to be used for wet work or when handling citrus fruits, potatoes, tomatoes, brinjals, papayas or when using polishes, paints or solvents. For outdoor work, leather work or for dry housework, cotton gloves to be used. For washing purpose, dishwasher/washing machine should be utilized, if available. Hands should be washes only with a mild soap and lukewarm water, after removing the rings. To prevent involvement of feet, a washing board, if work is carried out by standing or a low stool, if carried out in a squatting position is useful to prevent contact with soap and water.

The skin should be lubricated frequently with bland cream or lotion, in morning and then reapplied at lunch time and work breaks. Hands should be soaked for 5 minutes in water and a hydrophobic emollient immediately applied. High potency corticosteroids are needed in the treatment of chronic hand or foot dermatitis. UVB photochemotherapy can be extremely used in chronic or hand foot dermatitis. Prednisolone is given for severe eczematous hand dermatitis. Acrodermatitis enteropathica without treatment is fatal and affected individuals may die within a few years. There is no cure for the condition. Treatment includes lifelong dietary zinc supplementation in the range of greater than 1-2 mg/kg of bodyweight per day. The course of ACA is long-standing, from a few to several years, and it leads to extensive atrophy of the skin and, in some patients, to the limitation of upper and lower limb joint mobility.The outlook is good if the acute inflammatory stage of ACA is treated adequately. The therapeutic outcome is difficult to assess in patients with the chronic atrophic phase, in which many changes are only partially reversible.

ECZEMA-HOMOEOPATHIC POINT OF VIEW

Eczema, which is presented with some prominent and characteristic symptoms on skin, is a disease of much controversy and discussion. Even though, this chronic disease is presented with few symptoms, Dr.Hahnemann recognized its origin in basic dynamic force. The development of this disease and its treatment, were much discussed in the Organon of Medicine, although the name eczema was not mentioned. In the classification of diseases, Dr.Hahnemann points out the basic manifestation of this chronic disease, as the first manifestation of the chronic miasm, Psora. Dr.Hahnemann describes it in Aphorism 80, of the Organon of medicine, as “after the completion of the internal infection of the whole organism, announce by a peculiar cutaneous eruption, sometimes consisting only of a few vesicles accompanied by intolerable voluptuous tickling itching (and a peculiar odour),the monstrous internal chronic miasm-the Psora, the only real fundamental cause”.

In Aphorism 78, Dr.Hahnemann points out that, “The true natural chronic diseases are those that arise from a chronic miasm, which when left to themselves, and unchecked by the employment of those remedies that are specific for them, always go on increasing and growing worse, notwithstanding the best mental and corporeal regimen, and torment the patient to the end of his life with ever aggravated sufferings. These are the most numerous and greatest scourges of the human race; for the most robust constitution, the best regulated mode of living and the most vigorous energy of the vital force are insufficient for their eradication”. It is clear that even though the simple eruption started with itching, it go on attaining various forms of presentation as the time and circumstances allow. So considering eczema only as an affection of skin, is totally misleading. Every, skin affection is a valuable pointer to the chronic internal infection.

Even though the chronic disease originates with few cutaneous vesicles, it can progress into innumerable forms of disease. Likewise, eczema also progresses and developed into most incurable forms due to mishandling of this disease by modern medicine. That is why different forms of eczema are developing with different apparent etiology. This is pointed out by Dr.Hahnemann in Aphorism 187 of the Organon of medicine,” But those affections, alterations and ailments appearing on the external parts, that do not arise from any external injury or that have only some slight external wound for their immediate exciting cause, are produced in quite another manner; their source lies in some internal malady. To consider them as mere local affections, and at the same time to treat them only, or almost only, as it were surgically, with topical applications-as the old school have done from the remotest ages-is as absurd as it is pernicious in its results.”

The dynamic origin of the eczema as all other chronic diseases was put forward by homoeopaths only. There are so many recordings regarding this in Homoeopathic literature. Dr.J.H.Allen in “The Chronic Miasms”, says: “The skin is the mirror or the reflector of the internal stress, the internal dynamis, the internal workings of this human machine. It has in the skin, its reflectors, its kaleidoscope, its kinetoscopic views of its internal movements and its multiple shadings of disease, its lights and its shadows, that go to make up a picture, thrown upon the human canvas, the skin, showing much of perverted life action in the organism.”

“We have in skin diseases and all external manifestation of disease, peripheral expression through nerve transmission. It is taken up from within and transferred outwardly as a relief process. This is Nature’s provisional safety valve.” By all these extracts, it is clear that Homoeopathy considers eczema, as a chronic, miasmatic disease, which invades the whole of the organism and express outwardly with skin symptoms.

“The chronic miasm which lie behind the eczema is to be carefully traced in each case. The basic miasm that lie behind eczema, at its beginning stage is Psora. The appearance of the disease at its first stage has typical psoric presentation. Eczema may have its basis in any of the chronic miasms but probably no other disease give a fuller and clearer conception of profound and persistent action of Psora, as does eczema presenting itself as it does in both sexes and in all ages, from the infant of a few days to old age. Few diseases have the pruritus of eczema, so characteristic of Psora. Its multiplicity of forms and the innumerable variety of its phenomena, besides the frequency with which it makes its appearance gives it the foremost place of interest and study to the dermatologists.”

“The most common psoric symptoms present in the eczema are vesicles of the itch with voluptuous tickling itching. Patient rubs and scratches, better for few moments, after which there is a long continued burning of the part affected. Late in the evening and before midnight, this itching is more frequent and most unbearable. Skin is dry, rough, dirty or unhealthy-looking. Papular eruption of eczema- usually very little suppuration; Anhidriosis; colour of the skin is not much changed”.

Even though the acute symptoms at its origin have a psoric base, when it becomes subacute and chronic, the invasions of other miasms are also evident. “The wondrous variations that we find in eczema are in themselves a miasmatic study and often a great problem to decipher as to their miasmatic origin, from the papular eruption of the Psora to the pustules of the pseudopsoric. In eczema exfoliate we see all the chronic miasms reflected there in and more particularly, the sycotic element.”

Syphilitic symptoms are “eruptions found about the joints, flexures of the body or arranged in circular groupings. No itching and very little soreness. Scales and crusts thick, heavy, patchy and in circumscribed spots.”

Sycotic symptom, present in, every advanced case of eczema, is very peculiar and should be noted because of the malignant stage of the disease. “Much scaling-which are patchy and in circumscribed spots. It is more seen in eczema exfoliate. Skin lesions in tertiary stage- All forms of facial skin diseases that are contracted in Barber’s shop except Tinea favosa, erythematous eczema.” Sycotic manifestations are characterized by slowness of recovery.

Pseudopsoric taint is obtained in the following symptoms:

Skin affections with glandular involvement.

Varicose veins-tubercular taint predominates.

In eczema-pustule.

“It is the tubercular diathesis that complicates all skin diseases and makes them so difficult to remove.” Every presenting symptom can be classified into, the corresponding miasm and we can assume the nature of the disease. In most cases, symptoms of all 3 miasms are present.

Homoeopathic management of eczema

According to Dr.Hahnemann, “local maladies signifies those changes and ailments that appear on the external parts of the body”, as mentioned in Aphorism 185 of the Organon of medicine. But strictly speaking, there cannot be any local disease, as any disturbance in the nature of a dynamic change is never confined to a specific part of the organism. Therefore, eczema cannot be regarded as merely a local affection and to treat it exclusively by local applications is absolutely erroneous and most detrimental to the health of the patient.

So, the treatment of eczema and all other local affections, must consist in the selection of a remedy which must be homoeopathic, not only to the character of those local affections but also to the totality of symptoms which the patient present-in which case the general morbid state is removed along with the local affection, proving that local affection should be considered as an inseparable part of the whole, as one of the most considerable and striking symptoms of the whole disease.

The treatment of local maladies is mentioned in Aphrisms194-209. If local maladies are treated solely by means of external applications, it leads to the rousing of the internal disease and other symptoms that previously existed in a latent state side by side with the local affection and it will be driven back to the system or upon the nerves, thereby increasing the internal disease and canalizing the disease force through other channels leading to derangement of other parts of the body. Further treatment also becomes difficult, as the totality of symptoms, have become so distorted, obscure and vague, and it becomes impossible to individualize the patient and select a similimum.

The persistence of the local affection, even after the removal of the symptoms, shows that, the local malady (eczema), always arise from an internal malady or derangement of the vital force. Therefore, the treatment of eczema should be done, only by the internal administration of suitable homoeopathic remedies, which will effect the annihilation and cure of the general malady. This is the only judious, sure, efficacious and radical treatment for local maladies.

Medicinal management

Kent’s repertory

Rubric: SKIN-ERUPTIONS-eczema

3mark:Ars, Ars-i, Bar-m, Calc, Calc-s, Cic, Crot-t, Dulc, Graph, Hep, Jug-c , Jug-r, Lappa, Mez, Olnd, Petr, Psor, Rhus-t, Sulph, Sulph-i.

2mark: Aur-m,Calad,Carb-v,Caust,Iris,Kali-ar,Kali-chl,Kali-s,Lith-c,Lyc,Merc,Nat-s,Phyt,Ran-b,Sars,Sep,Sil,Staph,Thuj,Viol-t

1mark: Alum, Am-c, Am-m, Anac, Ant-c, Arg-n, Astac, Aur, Bell, Borx, Brom, Bry, Canth, Carb-ac, Carbn-s, Clem, Cop, Cycl, Fl-ac, Hydr, Kali-bi, Kali-c, Lach, Led, Nat-m, Nat-p, Nit-ac, Phos, Rhus-v

Synthesis repertory

Rubric: SKIN-ERUPTIONS-eczema

5 mark :Anthraci, Ars, Ars-i, Bar-c, Bar-m, Bov, Calc, Calc-s, Cic, Crot-t, Graph, Hep, Jug-c, Jug-r, Lappa, Lyc, Med, Mez, Nat-m, Olnd, Petr, Phos, Psor, Rhus-t, Sep, Sul-i, Sulph, Tub

4mark: Alumn, Aur-m, Aur-m-n, Calad, Calc-p, Carb-v, Caust, Chel, Cist, Con, Hydrc,Iris, Kali-ar, Kali-chl, Kali-s, Kreos, Lith-c, Merc, Merc-c, Mur-ac, Nat-c, Nat-s, Phyt, Ran-b, Sars, Sil, Staphy, Syph, Thuj, Viol-t

3mark: Acon, Aeth, Aethi-a, Alum, Alum-p, Alum-sil, Am-c, Am-m, Anac, Ant-c, Ant-t, Aq-mar, Arb, Arg-n, Arn, Ars-s-f, Ars-s-r, Arum-t, Astac, Aur, Aur-ar, Bell, Berb-a, Borx, Brom, Bry, Bufo, Calc-sil, Canth, Carb-ac, Carbn-s, Carc, Cardios-h, Cere-b, Chin, Clem, Cod, Colch, Com, Cop, Corn, Corn-a, Cund, Cur, Cycl, Dys, Fago, Falco-pe, Ferr-i, Ferr-s, Fl-ac, Fuli, Furm, Ger-i, Hom-xyz, Hydr, Iodof, Kali-bi, Kali-br, Kali-c, Kali-i, Kali-m, Kali-sil, Lac-f, Lach, Led , Mang, Merc-i-r, Moni ,Morg, Morg-p, Naphtin, Nat-p, Nit-ac, Op, Osm, Ox-ac, Penic, Ph-ac, Pip-m, Pix polyg-xyz, Positr, Pot-e,  Prim-o, Prim-v, Puls, Pyrog, Rad-br, Rhus-d, Rhus-v, Sanic, Scroph-n, Skook, Solid, Spira, Streptoc, Strych-g, Sul-ac, Sumb, Tarent, Tarent-c, Tell, Ter, Thyr, Titan, Tub-d, Urt-u, Ust, Vac, Xero, Zinc.

Boericke’s repertory

2 mark: Aethiops, Anac, Ant.c, Ars, Berb.v, Bov, Calc.c, Canth, Carb.ac, Clem, Crot.t, Graph, Hep, Kali ars, Mang.ac, Merc.c, Merc.s, Mez, Oleand, Petrol, Plumb, Psor, Rhus.t, Rhus.v, Sep, Sul, Sul.i, Vinca, Viola.tr

1mark:Alnus, Alum, Anthrok, Arbut, Berb.aq, Bor, Caps, Carbo v, Castor eq, Caust, Chrysar, Commocl, Con, Dulc, Euphorb, Fluor.ac, Frax.am, Fuligo, Hippoz, Hydrocot, Jugl.c, Kali.m, Kreos, Lyc, Merc.d, Merc.pr.rub, Mur.ac, Nat. ars, Nat.m, Nux v, Persicaria, Pilocarp, Pod, Prim.v, Sars, Skook.ch, Thuja, Tub, Ustil, Xerophyl, X-ray

Indications of homoeopathic medicines

1. 1. Arsenicum album:

Skin is dry and scaly, cold, blue and wrinkled; with cold, clammy perspiration; like parchment; white and pasty; black vesicles and burning pain; the affected parts burn like fire, as if hot coals were applied to parts.The patient is mentally restless but physically too weak to move. Thinks disease is incurable and there is dread of death when alone. Great prostration, with rapid sinking of the vital forces. Great thirst for cold water; drinks often, but little at a time.

<: after midnight (1-2a.m or p.m); from cold; cold food or drinks; when lying on affected side or with head low.

>: by heat, hot drinks, and hot applications.

1. 2. Arsenicum iodatum:

Eczema of the beard; watery, oozing and itchy discharge  <: washing. Enlarged scrofulous glands. Dry, scaly and itching skin. Marked exfoliation of skin layers. Scales leave a raw exuding surface beneath. Debilitating night sweats.

1. 3. Calcarea carbonica:

Unhealthy skin, readily ulcerating; flaccid; small wounds do not heal readily. Glands swollen. Nettle rash >: cold air. Associated with coldness and sweat, on single parts. Head sweats profusely while sleeping, wetting pillow far around. Great longing for eggs.

1. 4. Calcarea sulphurica:

Unhealthy discharging pus; they do not heal rapidly. Yellow purulent crust or discharges. Purulent exudation in or upon the skin. Skin affections with yellow scabs. Many little matterless pimples under the hair, bleeding when scratched. Dry eczema in children.

1. 5. Cicuta virosa:

Eczema with no itching; exudation forms into a hard, lemon coloured crust. Pustules  which run together, forming thick, yellow scabs, on head and face. Suited to Sycosis menti or Barber’s itch. Brain disease from suppressed eruptions. Elevated eruptions as large as peas. Chronic impetigo.

<: touch, draughts, concussion, tobacco smoke.

1. 6. Croton tiglium:

Skin feels hide-bound. Intense itching of skin, but so tender is unable to scratch; >: by gentle rubbing. Develops an acute eczema over whole body. Pustular eruption, especially on face and genitals, with fearful itching, followed by painful burning. Vesicles; confluent, oozing. Vesicular erysipelas, itching exceedingly.

<: least food or drink; during summer; touch; night and morning; washing; from fruit and sweetmeats.

1. 7. Dulcamara:

Skin is delicate, sensitive to cold, liable to eruptions, especially urticaria; every time patient takes cold or is long exposed to cold. Rash appear before menses. Urticaria over whole body, no fever; itching burns after scratching; <: in warmth, >: in cold. Thick brown-yellow crusts on scalp, face, forehead, temples, chin; with reddish borders, bleeding when scratched. Pruritus always worse, in cold wet weather. Vesicular eruptions.

<: cold in general

>: external warmth

1. 8. Graphites :

Unhealthy skin; every injury suppurates; old cicatrices break open again; eruptions upon the ears, between fingers and toes and on various parts of the body, from which oozes a watery, transparent, sticky fluid. Eczema of lids; eruptions moist and fissured; lids red and margins covered with scales or crusts. The nails are brittle, crumbling, deformed; painful, sore, as if ulcerated; thick and crippled. Cracks or fissures, in ends of fingers, nipples, labial commissures; of anus, between the toes.

<: at night, during and after menstruation.

1. 9. Hepar sulphur:

The skin is very sensitive to touch, cannot bear even clothes to touch affected parts. Skin affections extremely sensitive to touch, the pain often causes fainting. Ulcers, herpes, surrounded by little pimples or pustules and spread by coalescing. Ulcers with bloody suppuration, smelling like old cheese. Ulcers very sensitive to contact, burning, stinging, easily bleeding. Sweats profusely day and night without relief. “Cold-sores” very sensitive. Cannot bear to be uncovered; wants to be wrapped up warmly. Chronic and recurring urticaria. The slightest injury causes suppuration. Indicated in angio-neurotic oedema.

10. Mezereum:

Eczema and itching eruptions after vaccination. Ulcers with thick yellowish-white scabs under which thick, yellow pus collects. Vesicles appears around the ulcers, itch violently, burn like fire; shining, fiery-red areola around. Linen or charpie sticks to the ulcers, they bleed when it is torn away. Eczema with intolerable itching, <: in bed and from touch; copious, serous exudation. The head is covered with thick, leather-like crust, under which thick and white pus collects here and there; hair is glued and matted together; pus after a time is ichorous, becomes offensive and breeds vermin. Child scratches face continuously, which is covered with blood; eruptions moist; itching worse at night; inflammatory redness of face.

<: cold air, cold washing, at night, touch or motion; bad effects of mercury or alcohol.

11. Petroleum :

Painful sensitiveness of skin of whole body; all clothing is painful; slight injury suppurates. Skin of hands rough, cracked; tip of fingers rough, cracked, fissured, every winter; tenderness of the feet, which are bathed in foul-smelling sweat. Painful, itching chilblains and chapped hands <: in cold weather, decubitus. Yellowish –green, thick crusts on face and neck, moist or amber coloured, discharge profuse, irritating the margins, pain on denuded surfaces like that of a slight burn, mainly on occiput, scrotum, perineum and thighs.

<: in winter, during a thunderstorm

12. Psorinum :

It is especially adapted to psoric constitutions. Indicated in chronic cases, when well selected remedies fail to relieve or permanently improve. The skin has an abnormal tendency to receive skin diseases; eruptions easily suppurate; dry, inactive, rarely sweats; dirty look, as if never washed; coarse, greasy, as if bathed in oil; bad effects from suppression by sulphur and zinc ointments.  The patient is driven to despair with excessive itching. Indolent ulcers slow to heal. Body has a filthy smell, even after bathing. Great sensitiveness to cold air or change of weather. Dry, scaly eruptions disappear in summer, return in winter. Feels unusually well day before attack. Discharges have

a carrion-like odour. Sleeplessness, from intolerable itching.

<: coffee, change of weather, cold, hot sunshine

>: heat, warm clothing even in summer

13. Rhustox :

Erysipelas, from left to right; vesicular, yellow vesicles; much swelling, inflammation; burning, itching, stinging. Moist eruptions, on head, beginning with small yellow vesicles with red areolae, forming thick crusts and hard horny scabs which eat off the hair, offensive itching,worse at night, surface raw, excoriated. They extend to shoulders, or eczema scrota on insides of thighs, discharging freely, or thickened, infiltrated and between the folds, sore and humid, <: by changes of weather, especially wet weather, in winter. Eczema of right hand. Cold, fresh air is not tolerated on head, making scalp painful.

14. Sulphur:

Indicated in dirty, filthy people, who are prone to skin affections.  When carefully selected remedies fail to produce a favourable effect especially in acute diseases, it frequently serves to rouse the reactive powers of the system. Indicated in complaints that are continually relapsing. Skin is dry, scaly, unhealthy, every little injury suppurates. Voluptuous itching, scratching>: “feels good to scratch”; scratching causes burning; <: from heat of bed; soreness in folds. Skin affections that have been treated by medicated soaps and washes. Aversion to being washed; always< after a bath.

<: at rest; when standing; warmth in bed; washing; bathing, changeable weather.

>: dry, warm weather, lying on the right side.

15. Alumina:

Dry, tettery, itching eruption, worse in winter; intolerable itching of whole body when getting warm in bed; scratches until bleeds, then becomes painful.

<: in cold air; during winter; while sitting; from eating potatoes; after eating soups; on alternated days; at new and full moon.

>: mild summer weather; from warm drinks; while eating; in wet weather.

16. Ammonium mur:

Useful in fat, bloated and lax persons who are indolent and sluggish; eruptions on hands; wrists and shoulders; skin peels off the fingers; blisters on fingers, especially on tips; skin intensely red, covered  with a fine brownish exfoliation, >: only by applying cold water day and night; anxious dreams with feeling of embarrassment;<: during menses with vomiting and diarrhea.

17. Anacardium:

Itching vesicles, rapidly becoming pustular, large, flat, later confluent, discharging a yellowish transparent fluid, hardening to a crust in the open air as the epidermis peels off, surface swollen, hyperaemic and suppurating, spreading from right to left and affecting chiefly fingers, eyelids, face, scrotum, chest and around neck; unbearable itching.

18. Antimonium crudum:

Eczema with gastric derangements. Suppurating , yellow-crusted eruption, painful to touch and easily detached; a green sanious pus oozes out from beneath the thick, hard, yellow crusts, irritating the surrounding parts, itching violently; <: from poultices,bathing, working in water, from alcoholic drinks and in the sun. Gastric derangement with violent thirst and mapped tongue. Eruptions especially on face, and genital organs; impetigo scroti.

19. Bovista:

Eczema of the back of hands(baker’s and grocer’s itch), especially when irritation is brought on by washing; moist vesicular eruption with formation of thick crusts, no relief from scratching; eruption about mouth and nostrils; general lassitude, especially about joints; flabby skin; foul perspiration.

20. Borax :

Unhealthy skin, slight injuries suppurate. Itching on back of finger joints. Erysipelatous with swelling and tension. Worse in cold weather.

21. Caladium:

Itching rash alternates with asthma. Burning sensation and erysipelatous inflammation. Sweet sweat attracts flies. Burning vesicular rash on chest, forearm and vulva. Great disinclination to move. Vertigo on going to sleep. Low-spirited, feels best when perspiring.

22. Cantharis :

Vesicular erysipelas; vesicles all over the bodywhich are sore and suppurating. Eczema solare with much burning and itching; when touched burning and smarting; complications with urinary troubles; eruptions begin in a small spot and spreads so as to involve a large surface, with a watery discharge underneath the scabs, >: from lying down and in cool weather, <: from warmth; scales form on scalp like enormous dandruff; hair falls out; perspiration smells urinous; eruption mostly on right side. Dermatitis venenata with blood formation. Secondary eczema about scrotum and genitals, following excessive perspiration.

<: touching, rubbing.

23. Carbo animalis:

Spongy ulcers, copper-coloured eruption. Chilblains, worse in evening, in bed and from cold.  Burning, rawness and fissures with moisture.

24. Carbo vegetabilis:

Itching worse on evening, when warm in bed. Moist skin. Hot perspiration. Ichorous offensive discharges.

25. Causticum :

Soreness in folds of skin, back of ears, between thighs. Cicatrices especially burns, scalds, freshen up, become sore again.

26. Juglans cinerea:

Eczema of hands and wrists, one attack hardly subsiding before another sets in; ichor oozing out when using hands, with intolerable itching and soreness, depriving patient of sleep; dyspepsia with bronchial irritation and cough; scrofulous swelling of glands.

27. Juglans regia :

Crusta lacteal with soreness around ears. Itching and eruptions of small red pustules. Scalp red and violently itches at night.

28. Kali Arsenicum:

Inveterate skin diseases. Dry, chronic eczema; skin of arms thicker and rougher, itching and tingling when getting warm, intensely fissured about joints, occasionally <: with eruption of distinct vesicles, warmth.

29. Lappa major:

Eruptions on head, face, neck and extremities. Moist, badly smelling, grayish-white crusts; most of hair gone and eruption extending to face.

30. Lycopodium:

Violent itching fissured eruptions. Chronic eczema associated with urinary, hepatic and gastric complaints and bleeds easily. Eruptions begin on back of head and extends to face, also on hands, crusts thick, oozing a fetid moisture, full of deep rhagades, breeding lice, itching violently; cervical glands swollen; sallow, constipated children, disposed to intertrigo.

<: from 4-8 p.m, getting heated, from poultices

>: from cold air or uncovering the parts.

31. Mercurius :

Diseases of the skin with intolerable biting, itching, over body, as from insect bites. Skin almost constantly moist. Humid, fetid eruption; thick, yellow discharge or yellow crusts form on scalp, surrounded by an inflamed border. Great tendency to clammy sweat over the body; Crusta lacteal; ulcers with irregular shapes and undefined edges. Pimples around the main eruption.

<: evening, warmth of bed, wet damp weather

>: on scratching

32. Natrum muriaticum:

Eczema raw, red, inflamed, especially in edges of hair. Dry eruptions especially on margins of hair and bends of joints. White scaly scabs on forehead from ear to ear; thick scabs oozing pus and matting hair together, with rawness , soreness and smarting pain.

<: from eating too much salt, at seashore, or from ocean voyage, 10-11 a.m

>: when lying down

33. Oleander :

Vesicular eruption about the head of children, with smooth, shining surface, with drops of serum standing out here and there and scabs turning brown when dry; humid scaly eruption on back part of head and behind ears, with biting and itching, as from lice; skin gets raw by the rubbing of clothing; gnawing itching while undressing, skin sensitive and sore.

<: undressing, rest, friction of clothes.

34. Phytolacca:

Erythematous blotches slightly elevated, passing over into vesicles, itching, but too sore to allow any scratching, or made worse by scratching; skin hot and dry; barber’s itch; glands inflamed and swollen.

35. Rananculus bulbosus:

Vesicular eruption on face, as from a burn, smarts as if scalded; vesiculation followed by scabbing and this by a renewal of vesicles , attended by burning and itching and formation of hard, horny scabs; eruptions in clusters.

36. Sarsaparilla :

Rash from exposure to open air; dry, itch-like eruptions, prone to appear in spring; become crusty. Itching eruption of forehead during menses. In rhagades, skin cracked on hands and feet; pain and burning particularly on sides of fingers and toes; skin hard, indurated.

<: during hot summer months

37. Sepia :

Itching of skin of various spots; of external genitalia; is not > by scratching and is apt to burning. Worse in bends of elbows and knees. Eruption is dry or soon becomes moist and discharges offensive pus like fluid copiously, which becomes dry, cracks and exfoliates.

38. Silicea:

Unhealthy skin; every little injury suppurates. Itching, burning, offensive eruption behind ears, ending in scabs, discharging pus, also on scrotum and hands <: by scratching; spreading from back to head; itching pustules on scalp and neck very sensitive >:wrapping up warmly; pustules form and discharge copiously.

39. Staphysagria :

Eczema with yellow, acrid moisture which oozes from under crust. New vesicles form from contact of exudation. By scratching one place, itching ceases, but appears in another part. Eczema of hands, ears, face and body.

40. Sulphur iodatum:

Weeping eczema. Itching on ears, nose and urethra. Popular eruptions on face. Cold sores on lips. Boils on neck. Barber’s itch. Arms covered with itching rash. Hair feels as if erect.

41. Thuja :

Eruptions only on covered parts; worse after scratching. Very sensitive to touch. Nails crippled, brittle and soft. Sweat only on uncovered parts or all over except head. Profuse, sour smelling, fetid sweat at night.

42. Viola tricolor :

Intolerable itching of skin. Eruptions particularly over face and head with burning and itching <: at night. Thick scabs, which crack and exude a tenacious yellow pus. Eczema impetigonoides of the face. Eczema in children, especially of scalp, with swollen glands.

Rare remedies

1. 1. Aethiops mercurialis: Scrofulous affections; eruption flavus like herpetic and eczematous; painful, irritating and scabby eruptions.
2. 2. Arbutus andrachne: A remedy for eczema associated with gouty and rheumatic symptoms.
3. 3. Alnus: Chronic eczema with glandular enlargements.
4. 4. Anthrakokali : Useful in skin affections, cracks and ulcerations. Popular like eruption with a vesicular tendency especially on scrotum, hands, tibia, shoulder and dorsum of feet.
5. 5. Berberis aquifolium: Dry, rough, scaly eruptions on scalp extending to face and neck. Dry eczema.
6. 6. Chrysarobinum : Vesicular or squamous lesions associated with foul smelling discharge and crust formation, tending to become confluent and to give the appearance of a single crust covering the entire area. Violent itching in thighs, legs and ears. Dry scaly eruptions especially around eyes and ears. Scabs with pus  underneath.
7. 7. Comocladia dentata: Eczema of trunks and extremities, also pustular type; itches red. Deep ulcers with hard edges.

<: touch, warmth

>: open air, scratching

1. 8. Chininum sulph: Itching erythema, vesiculations, pustules. Great sensitiveness, shriveled skin.
2. 9. Fraxinus americana: Infantile eczema

10. Hippozaenium : Used in eczema associated with lymphatic swellings.

11. Manganum acteicum: Suppuration of skin around joints. Red elevated spots. Itching better scratching. Burning around ulcers. Chronic eczema associated with amenorrhea, worse at menstrual period or at menopause.

12. Pilocarpus : Dry eczema, excessive perspiration from all parts of body. Chilliness with sweat.

13. Primula obonica: Moist eczema of face, pustular eruption on chin. Burns at night. Eyelids swollen; urticaria like eruption; eczema on arms, wrists, forearms, hands; popular and excoriated; great itching<: at night; small papules on a raised base. Skin symptoms accompanied by febrile symptoms.

14. Pix liquid: Skin cracked, itches intolerably, bleeds on scratching. Eruptions on back of hands.

15. Scrophularia nodosa: Prickling, itching, worse at back of hand.

16. Xerophyllum : Eczema with vesiculation, itching, stinging and burning. Blisters, little lumps. Skin rough and cracked; feels like leather. Dermatitis around knees.

<: cold water application

>: hot water application

17. X-ray: Dry, itching eczema. Erythema around roots of nails. Skin dry, wrinkled, painful cracks.

<: evening, night and in bed.

Acute form of eczema: chininum sulph, Rhustox, croton tig

Eczema behind ears: chrysarobinum, graphites, hepar sulph, Mezereum, oleander, scrophularia

Eczema of face: carbolic acid, croton tig, sulphur, suphur iodatum, vinca minor.

Eczema of flexures of joints: aethusa, graphites, hepar sulph, petroleum, pix liquid

Eczema of pudendum; croton tig

Eczema of rheumatic persons: Rhustox

Eczema of scalp: Calcarea carb, oleander, selenium, vinca minor

Eczema of strumous persons: aethiops. Arsenicum iodide, Calcarea iodide, hepar sulph

Eczema of whole body: croton tig, Rhustox

Eczema madidans: Cicuta, conium mac, Dulcamara, graphites, hepar sulph, kali mur, merc cor, mezeruem,sepia, tuberculinum

Eczema with pigmentation in circumscribed areas following: bereberis vulgaris

Eczema with urinary, hepatic, amnd gastric disorders: Lycopodium

Eczema worse after vaccination: mezereum

Eczema worse at sea shore, ocean voyages, excess salt: natrum mur.

CONCLUSION

Eczema is not a disease entity, but rather a reaction of the skin to varied and complex internal and external factors. Its precise etiology is unknown. The clinical syndrome results from interplay, between endogenous factors and environmental factors. The clinical picture varies according to the type of eczema and site of the body involved. Although recent advances in medicine have brought changing ideas, the treatment of eczema and its permanent cure is still a paradox. The emerging concept of “living with eczema,” or rather palliative or suppressive measures, shows that, modern medicine has not, actually changed over centuries and are still toiling in darkness, prevailing as in the times of our master, Dr. Hahnemann. Only homoeopathy, can assure better times for mankind, to tide over this trivial yet distressing ailment with its crystal clear concepts of disease causation and cure. While the orthodox medicine is still staggering behind with its palliative measure, Homoeopathy has time and again proved that it is the only rational, safe and judicious method of healing, through its wonderful cure of cases, over the years.

BIBLIOGRAPHY

1. Gray’s Textbook of Anatomy
2. Concise Medical Physiology by Chaudhari
3. Human Embryology by Inderbir Singh
4. Harrison’s Principles of Internal Medicine
5. Kumar&Clarke’s Clinical Medicine
6. Davidson’s Principles&Practice of Medicine
7. Panda’s Textbook of Medicine by U.N.Panda
8. Textbook of Medicine by K.V.Krishnadas
9. Practice of Dermatology by P.N.Behl

10.  IADVL Textbook and Atlas of Dermatolgy by R.G.Valia

11.  Textbook of Dermatology by Arthur Rook, D.S.Wilkinson, F.J.G.Ebling

12.  Practical Dermatology by I.B.Sneddon&R.E.Church

13.  Allen’s keynotes

14.  Pocket Manual of Homoeopatic Materia Medica& Repertory by William Boericke

15.  Homoeopathic therapeutics by Lilienthal

16.  Organon of Medicine by Samuel Hahnemann

17.  The Chronic Diseases,their peculiar nature& their homoeopathic cure by Dr. Samuel Hahnemann

18.  The Chronic Miasms by J.H.Allen

19.  www.dermnetz.org

20.  www.karger.com

21.  www.medicinenet.com

22.  www.emedicinehealth.com

23.  www.webmd.com

24.  www.nlm.nih.gov/medlineplus

25.  www.wrongdiagnosis.com